greenmedinfo--2020-04-17--Photoimmunology: how ultraviolet radiation affects the immune system.

Ultraviolet ( UV ) radiation is a ubiquitous component of the environment that has important effects on a wide range @ @ @ @ @ UVB radiation induces sunburn and is a potent immunomodulator , yet longer-wavelength , lower-energy UVA @ @ @ @ @ mammalian immunity .
This Review discusses current knowledge regarding the mechanisms by which UV radiation @ @ @ @ @ immune responses and how this immunomodulatory capacity can be both beneficial in the case of @ @ @ @ @ and detrimental in the case of skin cancer and the response to several infectious agents @

Ultraviolet (UV) radiation is a ubiquitous component of the environment that has important effects on a wide range of cell functions. Short-wavelength UVB radiation induces sunburn and is a potent immunomodulator, yet longer-wavelength, lower-energy UVA radiation also has effects on mammalian immunity. This Review discusses current knowledge regarding the mechanisms by which UV radiation can modify innate and adaptive immune responses and how this immunomodulatory capacity can be both beneficial in the case of inflammatory and autoimmune diseases, and detrimental in the case of skin cancer and the response to several infectious agents.


greenmedinfo--2020-04-17--Western diet and the immune system: An inflammatory connection.

The consumption of Western-type calorically rich diets combined with chronic overnutrition and a sedentary lifestyle in Western societies evokes a @ @ @ @ @ , termed metaflammation .
Metaflammation contributes to the development of many prevalent non-communicable diseases ( @ @ @ @ @ lifestyle-associated pathologies represent a rising public health problem with global epidemic dimensions .
A better @ @ @ @ @ and Western diet ( WD ) activate immune cells is essential for the development of @ @ @ @ @ for common NCDs .
Here , we review the current mechanistic understanding of how the @ @ @ @ @ , and we discuss how this knowledge can be translated to protect the public from @ @ @ @ @ their selected lifestyle .

The consumption of Western-type calorically rich diets combined with chronic overnutrition and a sedentary lifestyle in Western societies evokes a state of chronic metabolic inflammation, termed metaflammation. Metaflammation contributes to the development of many prevalent non-communicable diseases (NCDs), and these lifestyle-associated pathologies represent a rising public health problem with global epidemic dimensions. A better understanding of how modern lifestyle and Western diet (WD) activate immune cells is essential for the development of efficient preventive and therapeutic strategies for common NCDs. Here, we review the current mechanistic understanding of how the Western lifestyle can induce metaflammation, and we discuss how this knowledge can be translated to protect the public from the health burden associated with their selected lifestyle.


greenmedinfo--2020-04-17--The impact of dietary components on regulatory T cells and disease.

The rise in the prevalence of autoimmune diseases in developed societies has been associated with a change in lifestyle patterns .
Among other factors , increased consumption of certain dietary components , such as table salt and fatty acids and excessive caloric intake has been associated with defective immunological tolerance .
Dietary nutrients have shown to modulate the immune response by a direct effect on the function of immune cells or , indirectly , by acting on the microbiome of the gastrointestinal tract .
FOXP3regulatory T cells ( Tregs ) suppress immune responses and are critical for maintaining peripheral tolerance @ @ @ @ @ @ @ inflammation and autoimmune disease .
It is now well-recognized that Tregs show certain degree of plasticity and can gain effector functions to adapt their regulatory function to different physiological situations during an immune response .
However , plasticity of Tregs might also result in conversion into effector T cells that may contribute to autoimmune pathogenesis .
Yet , which environmental cues regulate Treg plasticity and function is currently poorly understood , but it is of significant importance for therapeutic purposes .
Here we review the current understanding on the effect of certain dietary @ @ @ @ @ @ @ metabolism , stability , and function .
Moreover , we will discuss the role of Tregs linking diet and autoimmunity and the potential of dietary-based interventions to modulate Treg function in disease .

The rise in the prevalence of autoimmune diseases in developed societies has been associated with a change in lifestyle patterns. Among other factors, increased consumption of certain dietary components, such as table salt and fatty acids and excessive caloric intake has been associated with defective immunological tolerance. Dietary nutrients have shown to modulate the immune response by a direct effect on the function of immune cells or, indirectly, by acting on the microbiome of the gastrointestinal tract. FOXP3regulatory T cells (Tregs) suppress immune responses and are critical for maintaining peripheral tolerance and immune homeostasis, modulating chronic tissue inflammation and autoimmune disease. It is now well-recognized that Tregs show certain degree of plasticity and can gain effector functions to adapt their regulatory function to different physiological situations during an immune response. However, plasticity of Tregs might also result in conversion into effector T cells that may contribute to autoimmune pathogenesis. Yet, which environmental cues regulate Treg plasticity and function is currently poorly understood, but it is of significant importance for therapeutic purposes. Here we review the current understanding on the effect of certain dietary nutrients that characterize Western diets in Treg metabolism, stability, and function. Moreover, we will discuss the role of Tregs linking diet and autoimmunity and the potential of dietary-based interventions to modulate Treg function in disease.


greenmedinfo--2020-04-16--Consumption of the total Western diet promotes colitis and inflammation-associated colorectal cancer

Consumption of the total Western diet promotes colitis and inflammation-associated colorectal cancer in mice.

Consumption of a Western type diet is a known risk factor for colorectal cancer .
Our group previously developed the total Western diet ( TWD ) for rodents with energy and nutrient profiles that emulate a typical Western diet .
In this study , we tested the hypothesis that consumption of the TWD would enhance colitis , delay recovery from gut injury and promote colon tumorigenesis .
In multiple experiments using the azoxymethane + dextran sodium sulfate ormouse models of colitis-associated colorectal carcinogenesis ( CAC ) , we determined that mice fed TWD experienced more severe and more prolonged colitis @ @ @ @ @ @ @ AIN93G diet , ultimately leading to markedly enhanced colon tumorigenesis .
Additionally , this increased tumor response was attributed to the micronutrient fraction of the TWD , and restoration of calcium and vitamin D to standard amounts ameliorated the tumor-promoting effects of TWD .
Finally , exposure to the TWD elicited large scale , dynamic changes in mRNA signatures of colon mucosa associated with interferon ( IFN ) response , inflammation , innate immunity , adaptive immunity , and antigen processing pathways , among others .
Taken together , these observations indicate that @ @ @ @ @ @ @ , delayed recovery from gut injury , and enhanced colon tumorigenesis likely via extensive changes in expression of immune-related genes in the colon mucosa .

Consumption of a Western type diet is a known risk factor for colorectal cancer. Our group previously developed the total Western diet (TWD) for rodents with energy and nutrient profiles that emulate a typical Western diet. In this study, we tested the hypothesis that consumption of the TWD would enhance colitis, delay recovery from gut injury and promote colon tumorigenesis. In multiple experiments using the azoxymethane + dextran sodium sulfate ormouse models of colitis-associated colorectal carcinogenesis (CAC), we determined that mice fed TWD experienced more severe and more prolonged colitis compared to their counterparts fed the standard AIN93G diet, ultimately leading to markedly enhanced colon tumorigenesis. Additionally, this increased tumor response was attributed to the micronutrient fraction of the TWD, and restoration of calcium and vitamin D to standard amounts ameliorated the tumor-promoting effects of TWD. Finally, exposure to the TWD elicited large scale, dynamic changes in mRNA signatures of colon mucosa associated with interferon (IFN) response, inflammation, innate immunity, adaptive immunity, and antigen processing pathways, among others. Taken together, these observations indicate that consumption of the TWD markedly enhanced colitis, delayed recovery from gut injury, and enhanced colon tumorigenesis likely via extensive changes in expression of immune-related genes in the colon mucosa.


greenmedinfo--2020-04-16--Lactobacillus Brevis OPK-3 from kimchi prevents obesity and modulates the expression of adipogenic a

Lactobacillus Brevis OPK-3 from kimchi prevents obesity and modulates the expression of adipogenic and pro-inflammatory genes.

Our previous study reported that lactic acid bacteria ( OPK-3 ) isolated from kimchi ameliorated intracellular lipid accumulation in 3T3-L1 @ @ @ @ @ explored potential roles ofOPK-3 ( KLAB ) on preventing body weight gain and its effect @ @ @ @ @ adipose tissue .
Male C57BL/6 mice ( = 10 ) were divided into four groups @ @ @ @ @ water ( NDC ) , high-fat diet with distilled water ( HDC ) , high-fat @ @ @ @ @ ) or high-fat diet with KLAB .
The KLAB supplement resulted in significantly lower body @ @ @ @ @ tissue mass , and lower serum and hepatic TG levels than the HDC .
KLAB @ @ @ @ @ and real-time polymerase chain reaction ( PCR ) analysis showed significantly lower inflammatory cytokine mRNA @ @ @ @ @ .
These results suggest that the administration of KLAB inhibits the induction of inflammation in @ @ @ @ @ inhibition of weight gain .
Therefore , this study demonstrates the therapeutic and beneficial value @ @ @ @ @ the fermentation of kimchi .

Our previous study reported that lactic acid bacteria (OPK-3) isolated from kimchi ameliorated intracellular lipid accumulation in 3T3-L1 adipocyte. The current study explored potential roles ofOPK-3 (KLAB) on preventing body weight gain and its effect on the inflammatory response of adipose tissue. Male C57BL/6 mice (= 10) were divided into four groups: normal diet with distilled water (NDC), high-fat diet with distilled water (HDC), high-fat diet with L-ornithine (OTC) or high-fat diet with KLAB. The KLAB supplement resulted in significantly lower body weight, lower epididymal fat tissue mass, and lower serum and hepatic TG levels than the HDC. KLAB supplementation improved serum cytokines, and real-time polymerase chain reaction (PCR) analysis showed significantly lower inflammatory cytokine mRNA levels in epididymal adipose tissue. These results suggest that the administration of KLAB inhibits the induction of inflammation in adipose tissue along with the inhibition of weight gain. Therefore, this study demonstrates the therapeutic and beneficial value of this strain produced during the fermentation of kimchi.


greenmedinfo--2020-04-16--Effects of novel probiotics in a murine model of irritable bowel syndrome.

Background/Aims : Dysbiosis is an important factor in the pathogenesis of irritable bowel syndrome ( IBS ) .
Several studies have reported promising results using probiotics for the treatment of IBS .
This study evaluated the efficacy of novel probiotics isolated from Kimchi , a Korean fermented food , and the feces of healthy Vietnamese people in a murine model of IBS .
Methods : DK121 was isolated from Kimchi , andV4 andV7 were isolated from the feces of healthy Vietnamese people residing in Korea .
Forty rats were allocated to receive one of the study strains , a mixture @ @ @ @ @ @ @ .
After 5 days of administration , the rats were restrained in a cage to induce IBS .
The effects of the probiotics on IBS were analyzed by evaluating the stool weights and stool consistency scores .
Results : The primary outcome was analyzed upon the completion of a three-week experiment .
The rats in the V7 group showed lower stool weights than those in the control group at week 2 ( median : 1.10 [ V7 ] vs. 2.35 [ control ] , p=0.04 , Mann-Whitney U-test ) and week 3 ( @ @ @ @ @ @ @ 2.80 [ control ] , p=0.017 ) .
The rats in the DK121 ( median : 2.00 , p=0.007 ) , V7 ( median : 2.00 , p=0.004 ) , and mixture ( median : 1.50 , p=0.001 ) groups showed better stool consistency scores at week 2 than the control group ( median : 3.00 ) .
Conclusions : The novel probiotics have beneficial effects on defecation in a murine model of IBS .
Human studies confirming the efficacy are warranted .

Background/Aims: Dysbiosis is an important factor in the pathogenesis of irritable bowel syndrome (IBS). Several studies have reported promising results using probiotics for the treatment of IBS. This study evaluated the efficacy of novel probiotics isolated from Kimchi, a Korean fermented food, and the feces of healthy Vietnamese people in a murine model of IBS.
Methods: DK121 was isolated from Kimchi, andV4 andV7 were isolated from the feces of healthy Vietnamese people residing in Korea. Forty rats were allocated to receive one of the study strains, a mixture of the strains, or the vehicle. After 5 days of administration, the rats were restrained in a cage to induce IBS. The effects of the probiotics on IBS were analyzed by evaluating the stool weights and stool consistency scores.
Results: The primary outcome was analyzed upon the completion of a three-week experiment. The rats in the V7 group showed lower stool weights than those in the control group at week 2 (median: 1.10 [V7] vs. 2.35 [control], p=0.04, Mann-Whitney U-test) and week 3 (median: 1.10 [V7] vs. 2.80 [control], p=0.017). The rats in the DK121 (median: 2.00, p=0.007), V7 (median: 2.00, p=0.004), and mixture (median: 1.50, p=0.001) groups showed better stool consistency scores at week 2 than the control group (median: 3.00).
Conclusions: The novel probiotics have beneficial effects on defecation in a murine model of IBS. Human studies confirming the efficacy are warranted.


greenmedinfo--2020-04-16--The role of beneficial bacteria wall elasticity in regulating innate immune response.

BACKGROUND : Probiotics have great potential to contribute to development of healthy dietary regimes , preventive care , and an integrated approach to immunity-related disease management .
The bacterial wall is a dynamic entity , depending on many components and playing an essential role in modulating immune response .
The impact of cell wall elasticity on the beneficial effects of probiotic strains has not been sufficiently studied .
The aim was to investigate the effect of lactic acid bacteria ( LAB ) and bifidobacteria strains on phagocytic system cells ( macrophages ) as related to bacterial wall elasticity , estimated @ @ @ @ @ @ @ .
METHODS : We conducted studies on Balb/c line mice 18-20 g in weight using lyophilized strains of LAB-Lactobacillus acidophilus IMV B-7279 , Lactobacillus casei IMV B-7280 , Lactobacillus delbrueckii subsp .
bulgaricus IMV B-7281 , and bifidobacteria-Bifidobacterium animalis VKL and Bifidobacterium animalis VKB .
We cultivated the macrophages obtained from the peritoneal cavity of mice individually with the strains of LAB and bifidobacteria and evaluated their effect on macrophages , oxygen-dependent bactericidal activity , nitric oxide production , and immunoregulatory cytokines .
We used AFM scanning to estimate bacterial cell wall elasticity @ @ @ @ @ @ @ stimulating effect on the functional activity of macrophages and ability to produce NO/NO2 in vitro .
Lactobacilli strains increased the production of IL-12 and IFN-γ in vitro .
The AFM demonstrated different cell wall elasticity levels in various strains of LAB and bifidobacteria .
The rigidity of the cell walls among lactobacilli was distributed as follows : Lactobacillus acidophilus IMV B-7279 > Lactobacillus casei IMV B-7280 > Lactobacillus delbrueckii subsp .
bulgaricus IMV B-7281 ; among the strains of bifidobacteria : B. animalis VKB > B .
animalis VKL .
Probiotic strain survival @ @ @ @ @ @ @ cell wall elasticity and on the time of their joint cultivation .
CONCLUSION : LAB and bifidobacteria strains stimulate immune-modulatory cytokines and active oxygen and nitrogen oxide compound production in macrophages .
Strains with a more elastic cell wall according to AFM data demonstrated higher resistance to intracellular digestion in macrophages and higher level of their activation .
AFM might be considered as a fast and accurate method to assess parameters of probiotic strain cell wall to predict their immune-modulatory properties .

BACKGROUND: Probiotics have great potential to contribute to development of healthy dietary regimes, preventive care, and an integrated approach to immunity-related disease management. The bacterial wall is a dynamic entity, depending on many components and playing an essential role in modulating immune response. The impact of cell wall elasticity on the beneficial effects of probiotic strains has not been sufficiently studied. The aim was to investigate the effect of lactic acid bacteria (LAB) and bifidobacteria strains on phagocytic system cells (macrophages) as related to bacterial wall elasticity, estimated using atomic force microscopy (AFM).
METHODS: We conducted studies on Balb/c line mice 18-20 g in weight using lyophilized strains of LAB-Lactobacillus acidophilus IMV B-7279, Lactobacillus casei IMV B-7280, Lactobacillus delbrueckii subsp. bulgaricus IMV B-7281, and bifidobacteria-Bifidobacterium animalis VKL and Bifidobacterium animalis VKB. We cultivated the macrophages obtained from the peritoneal cavity of mice individually with the strains of LAB and bifidobacteria and evaluated their effect on macrophages, oxygen-dependent bactericidal activity, nitric oxide production, and immunoregulatory cytokines. We used AFM scanning to estimate bacterial cell wall elasticity.
RESULTS: All strains had a stimulating effect on the functional activity of macrophages and ability to produce NO/NO2 in vitro. Lactobacilli strains increased the production of IL-12 and IFN-γ in vitro. The AFM demonstrated different cell wall elasticity levels in various strains of LAB and bifidobacteria. The rigidity of the cell walls among lactobacilli was distributed as follows: Lactobacillus acidophilus IMV B-7279>Lactobacillus casei IMV B-7280>Lactobacillus delbrueckii subsp. bulgaricus IMV B-7281; among the strains of bifidobacteria: B. animalis VKB>B. animalis VKL. Probiotic strain survival in the macrophages depended on the bacterial cell wall elasticity and on the time of their joint cultivation.
CONCLUSION: LAB and bifidobacteria strains stimulate immune-modulatory cytokines and active oxygen and nitrogen oxide compound production in macrophages. Strains with a more elastic cell wall according to AFM data demonstrated higher resistance to intracellular digestion in macrophages and higher level of their activation. AFM might be considered as a fast and accurate method to assess parameters of probiotic strain cell wall to predict their immune-modulatory properties.


greenmedinfo--2020-04-16--Th17 cells as potential probiotic therapeutic targets in Inflammatory bowel diseases.

Inflammatory bowel diseases ( IBD ) are characterized by wasting and chronic intestinal inflammation triggered by various cytokine-mediated pathways .
In recent years , it was shown that T helper 17 ( Th17 ) cells are involved in the pathogenesis of IBD , which makes them an attractive therapeutic target .
Th17 cells preferentially produce interleukin ( IL ) -17A-F as signature cytokines .
The role of the interplay between host genetics and intestinal microbiota in the pathogenesis of IBD was demonstrated .
Probiotics are live microorganisms that when orally ingested in adequate amounts , confer a health benefit to @ @ @ @ @ @ @ or by stimulating the local immune system .
Several studies indicated the effectiveness of probiotics in preventing and treating IBD ( ulcerative colitis , and Crohn 's disease ) .
Furthermore , there is mounting evidence of probiotics selectively targeting the Th17 lineage in the prevention and management of inflammatory and autoimmune diseases such as IBD .
This review highlights critical roles of Th17 cells in the pathogenesis of IBD and the rationale for using probiotics as a novel therapeutic approach for IBD through manipulation of Th17 cells .
The potential molecular mechanisms @ @ @ @ @ @ @ and production are also discussed .

Inflammatory bowel diseases (IBD) are characterized by wasting and chronic intestinal inflammation triggered by various cytokine-mediated pathways. In recent years, it was shown that T helper 17 (Th17) cells are involved in the pathogenesis of IBD, which makes them an attractive therapeutic target. Th17 cells preferentially produce interleukin (IL)-17A-F as signature cytokines. The role of the interplay between host genetics and intestinal microbiota in the pathogenesis of IBD was demonstrated. Probiotics are live microorganisms that when orally ingested in adequate amounts, confer a health benefit to the host by modulating the enteric flora or by stimulating the local immune system. Several studies indicated the effectiveness of probiotics in preventing and treating IBD (ulcerative colitis, and Crohn's disease). Furthermore, there is mounting evidence of probiotics selectively targeting the Th17 lineage in the prevention and management of inflammatory and autoimmune diseases such as IBD. This review highlights critical roles of Th17 cells in the pathogenesis of IBD and the rationale for using probiotics as a novel therapeutic approach for IBD through manipulation of Th17 cells. The potential molecular mechanisms by which probiotics modulate Th17 cells differentiation and production are also discussed.


greenmedinfo--2020-04-17--Chamomile Oil for Carpal Tunnel Syndrome

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greenmedinfo--2020-04-17--Ultraviolet irradiation of skin alters the faecal microbiome independently of vitamin D.

Reduced sunlight exposure has been associated with an increased incidence of Crohn 's disease and ulcerative colitis .
The effect of ultraviolet radiation ( UVR ) on the faecal microbiome and susceptibility to colitis has not been explored .
C57Bl/6 female mice were fed three different vitamin D-containing diets for 24 days before half of the mice in each group were UV-irradiated ( 1 kJ/m² ) for each of four days , followed by twice-weekly irradiation of shaved dorsal skin for 35 days .
Faecal DNA was extracted and high-throughput sequencing of the 16S RNA gene performed .
UV irradiation @ @ @ @ @ @ @ change in the beta-diversity of faeces compared to nonirradiated mice , independently of vitamin D. Specifically , members of phylum Firmicutes , including , were enriched , whereas members of phylum Bacteroidetes , such as Bacteroidales , were depleted .
Expression of colonicincreased by four-fold anddecreased by five-fold , suggesting a UVR-induced anti-inflammatory effect .
UV-irradiated mice , however , were not protected against colitis induced by dextran sodium sulfate ( DSS ) , although distinct faecal microbiome differences were documented post-DSS between UV-irradiated and nonirradiated mice .
Thus , skin exposure to @ @ @ @ @ @ @ further investigations to explore the implications of this in health and disease are warranted .

Reduced sunlight exposure has been associated with an increased incidence of Crohn's disease and ulcerative colitis. The effect of ultraviolet radiation (UVR) on the faecal microbiome and susceptibility to colitis has not been explored. C57Bl/6 female mice were fed three different vitamin D-containing diets for 24 days before half of the mice in each group were UV-irradiated (1 kJ/m²) for each of four days, followed by twice-weekly irradiation of shaved dorsal skin for 35 days. Faecal DNA was extracted and high-throughput sequencing of the 16S RNA gene performed. UV irradiation of skin was associated with a significant change in the beta-diversity of faeces compared to nonirradiated mice, independently of vitamin D. Specifically, members of phylum Firmicutes, including, were enriched, whereas members of phylum Bacteroidetes, such as Bacteroidales, were depleted. Expression of colonicincreased by four-fold anddecreased by five-fold, suggesting a UVR-induced anti-inflammatory effect. UV-irradiated mice, however, were not protected against colitis induced by dextran sodium sulfate (DSS), although distinct faecal microbiome differences were documented post-DSS between UV-irradiated and nonirradiated mice. Thus, skin exposure to UVR alters the faecal microbiome, and further investigations to explore the implications of this in health and disease are warranted.


greenmedinfo--2020-04-17--Sub-erythemal ultraviolet radiation can increase the diversity of the gut microbiome, which in turn

Sub-erythemal ultraviolet radiation can increase the diversity of the gut microbiome, which in turn may be beneficial to the health of the host.

Many alterations to the skin microbiome by exposure to UV radiation ( UVR ) have been postulated and may contribute to the ability of UVR phototherapy to regulate skin inflammatory diseases .
Very recently , an effect of sub-erythemal narrowband UVB radiation ( 311 nm ) on the gut microbiome of healthy individuals was reported .
The relative abundance of Firmicutes and Proteobacteria increased in faecal samples of those receiving three exposures to narrowband UVB radiation ; the Bacteroidetes phyla were reduced by UVB .
In mice chronically exposed to sub-erythemal broadband UVR , similar faecal changes in Firmicutes and @ @ @ @ @ @ @ have allowed a further dissection of the relative ability of UVR and dietary vitamin D to modulate the gut microbiome by analysis of relative bacterial abundance in mice with similar 25-hydroxy vitamin D levels obtained by UVR exposure or from their diet , respectively .
The studies of mice recovering from colitis suggested that dietary vitamin D could stimulate greater faecal abundance of Rikenellaceae , whilst exposure to UVR was necessary for changes to the abundance of Lachnospiraceae and Desulfovibrionaceae .
Both human and murine studies report that multiple exposures to sub-erythemal UVR @ @ @ @ @ @ @ microbiome , which in turn may be beneficial to the health of the host .

Many alterations to the skin microbiome by exposure to UV radiation (UVR) have been postulated and may contribute to the ability of UVR phototherapy to regulate skin inflammatory diseases. Very recently, an effect of sub-erythemal narrowband UVB radiation (311 nm) on the gut microbiome of healthy individuals was reported. The relative abundance of Firmicutes and Proteobacteria increased in faecal samples of those receiving three exposures to narrowband UVB radiation; the Bacteroidetes phyla were reduced by UVB. In mice chronically exposed to sub-erythemal broadband UVR, similar faecal changes in Firmicutes and Bacteroidetes have been reported. Murine studies have allowed a further dissection of the relative ability of UVR and dietary vitamin D to modulate the gut microbiome by analysis of relative bacterial abundance in mice with similar 25-hydroxy vitamin D levels obtained by UVR exposure or from their diet, respectively. The studies of mice recovering from colitis suggested that dietary vitamin D could stimulate greater faecal abundance of Rikenellaceae, whilst exposure to UVR was necessary for changes to the abundance of Lachnospiraceae and Desulfovibrionaceae. Both human and murine studies report that multiple exposures to sub-erythemal UVR can increase the diversity of the gut microbiome, which in turn may be beneficial to the health of the host.


greenmedinfo--2020-04-17--Both vitamin D and ultraviolet radiation exposure can be considered potential master regulators of g

Both vitamin D and ultraviolet radiation exposure can be considered potential master regulators of gastrointestinal immunity.

: Environmental factors and an altered fecal microbiome are believed to be central to the pathogenesis of inflammatory bowel diseases ( IBD ) .
Vitamin D and ultraviolet radiation ( UVR ) are environmental factors that are associated by several pathways , including changes to the gastrointestinal microbiome , with the development and course of IBD .
: This review explores the interaction of vitamin D , and UVR , with the intestinal innate and adaptive immune systems , and how they may influence the gut microbiome and the subsequent development , and progression , of IBD .
: Vitamin @ @ @ @ @ @ @ adaptive immunity through a combination of common and independent mechanisms , with the overall effect being the promotion of immune tolerance .
Vitamin D , and to a lesser extent UVR , can modify the gastrointestinal microbiome either directly , or through immune-mediated mechanisms and this may explain the effect on intestinal inflammation in animal models of IBD and some clinical studies .
Thus , both vitamin D and UVR exposure can be considered potential 'master regulators ' of gastrointestinal immunity , fine-tuning the complex interaction between genetics , host immunity and the @ @ @ @ @ @ @ understanding of environment-host interactions is essential to achieving the ultimate goal of preventing and curing IBD .

: Environmental factors and an altered fecal microbiome are believed to be central to the pathogenesis of inflammatory bowel diseases (IBD). Vitamin D and ultraviolet radiation (UVR) are environmental factors that are associated by several pathways, including changes to the gastrointestinal microbiome, with the development and course of IBD.: This review explores the interaction of vitamin D, and UVR, with the intestinal innate and adaptive immune systems, and how they may influence the gut microbiome and the subsequent development, and progression, of IBD.: Vitamin D and UVR both regulate innate and adaptive immunity through a combination of common and independent mechanisms, with the overall effect being the promotion of immune tolerance. Vitamin D, and to a lesser extent UVR, can modify the gastrointestinal microbiome either directly, or through immune-mediated mechanisms and this may explain the effect on intestinal inflammation in animal models of IBD and some clinical studies. Thus, both vitamin D and UVR exposure can be considered potential 'master regulators' of gastrointestinal immunity, fine-tuning the complex interaction between genetics, host immunity and the gut microbiome. Further research and increased understanding of environment-host interactions is essential to achieving the ultimate goal of preventing and curing IBD.


greenmedinfo--2020-04-17--Skin exposure to narrow band ultraviolet light modulates the human intestinal microbiome.

The recent worldwide rise in idiopathic immune and inflammatory diseases such as multiple sclerosis ( MS ) and inflammatory bowel diseases ( IBD ) has been linked to Western society-based changes in lifestyle and environment .
These include decreased exposure to sunlight/UVB light and subsequent impairment in the production of vitamin D , as well as dysbiotic changes in the makeup of the gut microbiome .
Despite their association , it is unclear if there are any direct links between UVB light and the gut microbiome .
In this study we investigated whether exposing the skin to Narrow Band Ultraviolet @ @ @ @ @ @ @ serum vitamin D levels would also modulate the makeup of the human intestinal microbiota .
The effects of NB-UVB light were studied in a clinical pilot study using a healthy human female cohort ( = 21 ) .
Participants were divided into those that took vitamin D supplements throughout the winter prior to the start of the study ( VDS+ ) and those who did not ( VDS- ) .
After three NB-UVB light exposures within the same week , the serum 25 ( OH ) D levels of participants increased on average @ @ @ @ @ @ @ negatively correlated to the starting 25-hydroxy vitamin D [ 25 ( OH ) D ] serum concentration .
Fecal microbiota composition analysis using 16S rRNA sequencing showed that exposure to NB-UVB significantly increased alpha and beta diversity in the VDS- group whereas there were no changes in the VDS+ group .
Bacteria from several families were enriched in the VDS- group after the UVB exposures according to a Linear Discriminant Analysis ( LDA ) prediction , includingFamily , andThe serum 25 ( OH ) D concentrations showed a correlation with the relative abundance @ @ @ @ @ @ @ .
This is the first study to show that humans with low 25 ( OH ) D serum levels display overt changes in their intestinal microbiome in response to NB-UVB skin exposure and increases in 25 ( OH ) D levels , suggesting the existence of a novel skin-gut axis that could be used to promote intestinal homeostasis and health.clinicaltrials.gov , NCT03962673 .
Registered 23 May 2019 - Retrospectively registered , https : //clinicaltrials.gov/ct2/show/NCT03962673 ?
term=NCT03962673 & rank=1 .

The recent worldwide rise in idiopathic immune and inflammatory diseases such as multiple sclerosis (MS) and inflammatory bowel diseases (IBD) has been linked to Western society-based changes in lifestyle and environment. These include decreased exposure to sunlight/UVB light and subsequent impairment in the production of vitamin D, as well as dysbiotic changes in the makeup of the gut microbiome. Despite their association, it is unclear if there are any direct links between UVB light and the gut microbiome. In this study we investigated whether exposing the skin to Narrow Band Ultraviolet B (NB-UVB) light to increase serum vitamin D levels would also modulate the makeup of the human intestinal microbiota. The effects of NB-UVB light were studied in a clinical pilot study using a healthy human female cohort (= 21). Participants were divided into those that took vitamin D supplements throughout the winter prior to the start of the study (VDS+) and those who did not (VDS-). After three NB-UVB light exposures within the same week, the serum 25(OH)D levels of participants increased on average 7.3 nmol/L. The serum response was negatively correlated to the starting 25-hydroxy vitamin D [25(OH)D] serum concentration. Fecal microbiota composition analysis using 16S rRNA sequencing showed that exposure to NB-UVB significantly increased alpha and beta diversity in the VDS- group whereas there were no changes in the VDS+ group. Bacteria from several families were enriched in the VDS- group after the UVB exposures according to a Linear Discriminant Analysis (LDA) prediction, includingFamily, andThe serum 25(OH)D concentrations showed a correlation with the relative abundance of the, specifically members of theandgenera. This is the first study to show that humans with low 25(OH)D serum levels display overt changes in their intestinal microbiome in response to NB-UVB skin exposure and increases in 25(OH)D levels, suggesting the existence of a novel skin-gut axis that could be used to promote intestinal homeostasis and health.clinicaltrials.gov, NCT03962673. Registered 23 May 2019 - Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT03962673?term=NCT03962673&rank=1.


greenmedinfo--2020-04-17--Observational studies show an inverse association between vitamin D levels and development of food a

PURPOSE OF REVIEW : To review recent evidence on the capacity of vitamin D to prevent atopic disease , focussing on food allergy and asthma , and potential underlying mechanisms .
RECENT FINDINGS : The incidence of allergic disease continues to increase worldwide .
Vitamin D status is influenced by sun exposure and dietary intake .
Vitamin D deficiency is linked to an increased incidence of allergic disease and asthma .
These associations are generally strongest in early life .
The capacity of vitamin D to enhance antimicrobial pathways , promote peripheral immunological tolerance and maintain mucosal barrier integrity may @ @ @ @ @ @ @ addressed the capacity of vitamin D supplementation in utero and early life to reduce the incidence of disease .
Ancillary studies have provided insights into potential biological mechanisms linked to these effects .
SUMMARY : Observational studies show an inverse association between vitamin D levels and development of food allergy and asthma .
Secondary analyses of two recent interventional studies suggest that achieving vitamin D sufficiency throughout pregnancy reduces the incidence of asthma/recurrent wheeze at 3 years .
Longitudinal studies of vitamin D requirements in utero and postnatally , better understanding of factors @ @ @ @ @ @ @ mechanistic insights into vitamin D effects on neonatal-specific immune pathways are awaited .

PURPOSE OF REVIEW: To review recent evidence on the capacity of vitamin D to prevent atopic disease, focussing on food allergy and asthma, and potential underlying mechanisms.
RECENT FINDINGS: The incidence of allergic disease continues to increase worldwide. Vitamin D status is influenced by sun exposure and dietary intake. Vitamin D deficiency is linked to an increased incidence of allergic disease and asthma. These associations are generally strongest in early life. The capacity of vitamin D to enhance antimicrobial pathways, promote peripheral immunological tolerance and maintain mucosal barrier integrity may underlie these associations. Interventional studies have addressed the capacity of vitamin D supplementation in utero and early life to reduce the incidence of disease. Ancillary studies have provided insights into potential biological mechanisms linked to these effects.
SUMMARY: Observational studies show an inverse association between vitamin D levels and development of food allergy and asthma. Secondary analyses of two recent interventional studies suggest that achieving vitamin D sufficiency throughout pregnancy reduces the incidence of asthma/recurrent wheeze at 3 years. Longitudinal studies of vitamin D requirements in utero and postnatally, better understanding of factors that influence bioavailability of vitamin D and mechanistic insights into vitamin D effects on neonatal-specific immune pathways are awaited.


greenmedinfo--2020-04-17--Hydrocortisone and ascorbic acid synergistically prevent and repair lipopolysaccharide-induced pulmo

Hydrocortisone and ascorbic acid synergistically prevent and repair lipopolysaccharide-induced pulmonary endothelial barrier dysfunction.

BACKGROUND : Sepsis refers to the dysregulated host immune response elicited by microbial infections resulting in life-threatening organ dysfunction .
Sepsis represents a medical challenge , since it is associated with a rate of death as high as 60 % .
Septic shock is strongly associated with vascular dysfunction and elevated pulmonary capillary permeability .
We recently reported that the combination of hydrocortisone ( HC ) , ascorbic acid ( vitC ) , and thiamine dramatically improves outcomes and reduces mortality in patients with sepsis .
In the present study , we provide experimental evidence in support of the hypothesis @ @ @ @ @ @ @ enhances endothelial barrier function .
METHODS : Human lung microvascular endothelial cells were exposed to lipopolysaccharide ( LPS ) in the absence or presence of HC and vitC .
RESULTS : LPS alone induced profound hyperpermeability , as reflected in decreased values of transendothelial electrical resistance .
vitC alone did not exhibit barrier enhancement properties nor did it affect the LPS-induced hyperpermeability .
Similarly , HC alone exhibited only a minor barrier-enhancing and protective effect .
Conversely , the combination of HC and vitC , either as beforeor after treatment , dramatically reversed @ @ @ @ @ @ @ effects of HC and vitC were associated with reversal of LPS-induced p53 and phosphorylated cofilin downregulation and LPS-induced RhoA activation and myosin light chain phosphorylation .
CONCLUSIONS : These data provide a novel mechanism of endothelial barrier protection and suggest one possible pathway that may contribute to the therapeutic effects of HC and vitC in patients with sepsis .

BACKGROUND: Sepsis refers to the dysregulated host immune response elicited by microbial infections resulting in life-threatening organ dysfunction. Sepsis represents a medical challenge, since it is associated with a rate of death as high as 60%. Septic shock is strongly associated with vascular dysfunction and elevated pulmonary capillary permeability. We recently reported that the combination of hydrocortisone (HC), ascorbic acid (vitC), and thiamine dramatically improves outcomes and reduces mortality in patients with sepsis. In the present study, we provide experimental evidence in support of the hypothesis that the combination of HC and vitC enhances endothelial barrier function.
METHODS: Human lung microvascular endothelial cells were exposed to lipopolysaccharide (LPS) in the absence or presence of HC and vitC.
RESULTS: LPS alone induced profound hyperpermeability, as reflected in decreased values of transendothelial electrical resistance. vitC alone did not exhibit barrier enhancement properties nor did it affect the LPS-induced hyperpermeability. Similarly, HC alone exhibited only a minor barrier-enhancing and protective effect. Conversely, the combination of HC and vitC, either as beforeor after treatment, dramatically reversed the LPS-induced barrier dysfunction. The barrier-protective effects of HC and vitC were associated with reversal of LPS-induced p53 and phosphorylated cofilin downregulation and LPS-induced RhoA activation and myosin light chain phosphorylation.
CONCLUSIONS: These data provide a novel mechanism of endothelial barrier protection and suggest one possible pathway that may contribute to the therapeutic effects of HC and vitC in patients with sepsis.


greenmedinfo--2020-04-17--Patterns of death in patients with sepsis and the use of hydrocortisone, ascorbic acid, and thiamine

Patterns of death in patients with sepsis and the use of hydrocortisone, ascorbic acid, and thiamine to prevent these deaths.

In general , patients with sepsis die from the host response to the infecting pathogen rather than from the infecting @ @ @ @ @ of death have been identified in sepsis , namely vasoplegic shock , single-organ respiratory failure @ @ @ @ @ [ ARDS ] ) , multi-system organ failure ( MSOF ) , and persistent MSOF @ @ @ @ @ with recurrent infections ( persistent inflammation-immunosuppression and catabolism syndrome [ PICS ] ) .
To @ @ @ @ @ adjunctive therapies that modulate the immune system have been tested ; these therapies that have @ @ @ @ @ have universally failed.We propose that the combination of hydrocortisone , intravenous ascorbic acid , and @ @ @ @ @ , which synergistically targets multiple pathways , restores the dysregulated immune system and organ injury @ @ @ @ @ of death and organ failure following sepsis .

In general, patients with sepsis die from the host response to the infecting pathogen rather than from the infecting pathogen itself. Four patterns of death have been identified in sepsis, namely vasoplegic shock, single-organ respiratory failure (acute respiratory distress syndrome [ARDS]), multi-system organ failure (MSOF), and persistent MSOF with ongoing inflammation and immunosuppression with recurrent infections (persistent inflammation-immunosuppression and catabolism syndrome [PICS]). To improve the outcome of sepsis adjunctive therapies that modulate the immune system have been tested; these therapies that have targeted specific molecules or pathways have universally failed.We propose that the combination of hydrocortisone, intravenous ascorbic acid, and thiamine (HAT therapy), which synergistically targets multiple pathways, restores the dysregulated immune system and organ injury, and reduces the risk of death and organ failure following sepsis.


greenmedinfo--2020-04-17--Changes in transcript, metabolite and antibody reactivity during the early protective immune respons

Changes in transcript, metabolite and antibody reactivity during the early protective immune response in humans to Mycobacterium tuberculosis infection.

BACKGROUND : Strategies to prevent Mycobacterium tuberculosis ( Mtb ) infection are urgently required .
This study aimed to identify correlates of protection against early Mtb infection .
METHODS : Two groups of Mtb-exposed contacts of TB patients were recruited and classified according to their Mtb infection status using Tuberculin skin test ( TST ; cohort 1 ) or QuantiFERON ( QFT ; cohort 2 .
A negative reading at baseline with a positive reading at follow-up classified TST or QFT converters and a negative reading at both time-points classified TST or QFT non-converters .
RNA-sequencing , Mtb proteome arrays @ @ @ @ @ @ @ profiling was performed .
RESULTS : Several genes were found to be differentially expressed at baseline between converters and non-converters prior to any signs of infection by current tests .
Gene set enrichment analysis revealed a distinct B cell gene signature in TST non-converters compared to converters .
When infection status was defined by QFT , enrichment of Type I IFN and antiviral gene signatures was observed .
A remarkable AUC of 1.0 was observed for IgA reactivity to Rv0134 and an AUC of 0.98 for IgA reactivity to both Rv0629c and Rv2188c @ @ @ @ @ @ @ an AUC of 0.96 and was markedly higher compared to TST non-converters .
We also identified several differences in metabolite profiles , including changes in biomarkers of inflammation , fatty acid metabolism , and bile acids .
Pantothenate ( Vitamin B5 ) was significantly increased in TST non-converters compared to converters at baseline ( q=0.0060 ) .
CONCLUSIONS : These data provide new insights into the early protective response to Mtb infection and possible avenues to interfere with Mtb infection including Vitamin B5 supplementation .

BACKGROUND: Strategies to prevent Mycobacterium tuberculosis (Mtb) infection are urgently required. This study aimed to identify correlates of protection against early Mtb infection.
METHODS: Two groups of Mtb-exposed contacts of TB patients were recruited and classified according to their Mtb infection status using Tuberculin skin test (TST; cohort 1) or QuantiFERON (QFT; cohort 2. A negative reading at baseline with a positive reading at follow-up classified TST or QFT converters and a negative reading at both time-points classified TST or QFT non-converters. RNA-sequencing, Mtb proteome arrays (IgG and IgA) and metabolic profiling was performed.
RESULTS: Several genes were found to be differentially expressed at baseline between converters and non-converters prior to any signs of infection by current tests. Gene set enrichment analysis revealed a distinct B cell gene signature in TST non-converters compared to converters. When infection status was defined by QFT, enrichment of Type I IFN and antiviral gene signatures was observed. A remarkable AUC of 1.0 was observed for IgA reactivity to Rv0134 and an AUC of 0.98 for IgA reactivity to both Rv0629c and Rv2188c. IgG reactivity to Rv3223c resulted in an AUC of 0.96 and was markedly higher compared to TST non-converters. We also identified several differences in metabolite profiles, including changes in biomarkers of inflammation, fatty acid metabolism, and bile acids. Pantothenate (Vitamin B5) was significantly increased in TST non-converters compared to converters at baseline (q=0.0060).
CONCLUSIONS: These data provide new insights into the early protective response to Mtb infection and possible avenues to interfere with Mtb infection including Vitamin B5 supplementation.


greenmedinfo--2020-04-17--These data suggest that pantothenic acid induces an accelerating effect of the normal healing proces

The effect of pantothenic acid supplementation and deficiency on wound healing was investigated over a one month postoperative period in rabbits .
The supplemented group was injected with pentothenate ( 20 mg/kg of body weight/24 h ) for three weeks and compared to a placebo group ( 0.5 ml of distilled water ) .
Deficient animals were fed with a pantothenate free diet also for three weeks .
These three experimental groups were matched against a control group .
The degree of wound healing was determined by the mean of postoperative breaking strength and wound fibroblast population changes .
Pantothenic @ @ @ @ @ @ @ served as control of pantothenate consumption .
With regard to these three parameters no significant difference has been found between placebo and controls .
The average urinary elimination in the pantothenic acid group was significantly higher as far as the pantothenate supplemented group was concerned , while the deficient group showed no significant decrease when compared to controls .
Chronic pre- and postoperative pantothenic acid supplementation significantly increased aponeurosis strength after surgery ; it improved slightly , but not significantly the strength of the skin .
Furthermore , the fibroblast content of the @ @ @ @ @ @ @ proliferation phase after pantothenic supplementation .
These data suggest that pantothenic acid induces an accelerating effect of the normal healing process .
The mechanism responsible for this improvement seems to be an increase in cellular multiplication during the first postoperative period .
But the exact intimate mechanism of the beneficial effect of pantothenate remains unclear .

The effect of pantothenic acid supplementation and deficiency on wound healing was investigated over a one month postoperative period in rabbits. The supplemented group was injected with pentothenate (20 mg/kg of body weight/24 h) for three weeks and compared to a placebo group (0.5 ml of distilled water). Deficient animals were fed with a pantothenate free diet also for three weeks. These three experimental groups were matched against a control group. The degree of wound healing was determined by the mean of postoperative breaking strength and wound fibroblast population changes. Pantothenic acid urinary excretion measured by gas chromatography served as control of pantothenate consumption. With regard to these three parameters no significant difference has been found between placebo and controls. The average urinary elimination in the pantothenic acid group was significantly higher as far as the pantothenate supplemented group was concerned, while the deficient group showed no significant decrease when compared to controls. Chronic pre- and postoperative pantothenic acid supplementation significantly increased aponeurosis strength after surgery; it improved slightly, but not significantly the strength of the skin. Furthermore, the fibroblast content of the scar became significantly greater during the fibroblast proliferation phase after pantothenic supplementation. These data suggest that pantothenic acid induces an accelerating effect of the normal healing process. The mechanism responsible for this improvement seems to be an increase in cellular multiplication during the first postoperative period. But the exact intimate mechanism of the beneficial effect of pantothenate remains unclear.


greenmedinfo--2020-04-17--The potential role of B5: A stitch in time and switch in cytokine.

The wound healing process is a multifaceted sequence of activities associated with tissue restoration .
Novel approaches for the perfection of wound healing have been determined as a stitch in time saves nine .
Dysregulation of the immune response is a key element in the pathogenesis of rheumatic diseases and serves as a potential target for novel therapeutic strategies .
Vitamin B5 ( VB5 ) , also known as pantothenate or '' anti-stress vitamin , '' is the precursor of coenzyme A , which is essential in every micro-organism .
Many pantothenic acid amides acquire persuasive antimicrobial activity .
Pantothenic @ @ @ @ @ @ @ and skin barrier enhancing potential .
Its deficiency leads to reduced cortisol production , increased arthritic pain , myalgia , fatigue , headache , depression , insomnia , and widespread '' proinflammatory '' effects on the immune-system .
VB5 triggers immune cells to produce cytokines and is multifunctional .
The paradoxical effect of VB5 on the switch of anti-inflammatory and proinflammatory cytokines has been revealed .
This review aims to present the long research journey of B5 as it is becoming a forerunner in the healing of wounds and in enhancing the immune @ @ @ @ @ @ @ implications .
As its role in healing a wound stitch is promising , amending the immune system damage too is a hopeful target .

The wound healing process is a multifaceted sequence of activities associated with tissue restoration. Novel approaches for the perfection of wound healing have been determined as a stitch in time saves nine. Dysregulation of the immune response is a key element in the pathogenesis of rheumatic diseases and serves as a potential target for novel therapeutic strategies. Vitamin B5 (VB5), also known as pantothenate or"anti-stress vitamin,"is the precursor of coenzyme A, which is essential in every micro-organism. Many pantothenic acid amides acquire persuasive antimicrobial activity. Pantothenic acid improves surgical wounds healing with moisturizing and skin barrier enhancing potential. Its deficiency leads to reduced cortisol production, increased arthritic pain, myalgia, fatigue, headache, depression, insomnia, and widespread"proinflammatory"effects on the immune-system. VB5 triggers immune cells to produce cytokines and is multifunctional. The paradoxical effect of VB5 on the switch of anti-inflammatory and proinflammatory cytokines has been revealed. This review aims to present the long research journey of B5 as it is becoming a forerunner in the healing of wounds and in enhancing the immune function, thus providing potentially important therapeutic implications. As its role in healing a wound stitch is promising, amending the immune system damage too is a hopeful target.


greenmedinfo--2020-04-17--Vitamin B1 helps to limit Mycobacterium tuberculosis growth via regulating innate immunity.

It is known that vitamin B1 ( VB1 ) has a protective effect against oxidative retinal damage induced by anti-tuberculosis @ @ @ @ @ remains unclear whether VB1 regulates immune responses during ( MTB ) infection .
We report @ @ @ @ @ protective immune response to limit the survival of MTB within macrophages andthrough regulation of peroxisome @ @ @ @ @ .
VB1 promotes macrophage polarization into classically activated phenotypes with strong microbicidal activity and enhanced @ @ @ @ @ expression at least in part by promoting nuclear factor-κB signaling .
In addition , VB1 @ @ @ @ @ metabolism and PPAR-γ integrates the metabolic and inflammatory signals regulated by VB1 .
Using both @ @ @ @ @ , we demonstrate that VB1 enhances anti-MTB activities in macrophages andby down-regulating PPAR-γ activity .
@ @ @ @ @ of VB1 in regulating innate immune responses against MTB and reveal novel mechanisms by which @ @ @ @ @ macrophages .

It is known that vitamin B1 (VB1) has a protective effect against oxidative retinal damage induced by anti-tuberculosis drugs. However, it remains unclear whether VB1 regulates immune responses during(MTB) infection. We report here that VB1 promotes the protective immune response to limit the survival of MTB within macrophages andthrough regulation of peroxisome proliferator-activated receptorγ (PPAR-γ). VB1 promotes macrophage polarization into classically activated phenotypes with strong microbicidal activity and enhanced tumor necrosis factor-α and interleukin-6 expression at least in part by promoting nuclear factor-κB signaling. In addition, VB1 increases mitochondrial respiration and lipid metabolism and PPAR-γ integrates the metabolic and inflammatory signals regulated by VB1. Using both PPAR-γ agonists and deficient mice, we demonstrate that VB1 enhances anti-MTB activities in macrophages andby down-regulating PPAR-γ activity. Our data demonstrate important functions of VB1 in regulating innate immune responses against MTB and reveal novel mechanisms by which VB1 exerts its function in macrophages.


greenmedinfo--2020-04-17--This study provides the molecular and metabolic bases to understand the impacts of Vitamin B1 on Myc

This study provides the molecular and metabolic bases to understand the impacts of Vitamin B1 on Mycobacterium bovis.

BACKGROUND : Vitamin B ( V ) is a crucial dietary nutrient and essential cofactor for several key enzymes in the regulation of cellular and metabolic processes , and more importantly in the activation of immune system .
To date , the precise role of Vin Mycobacterium tuberculosis remains to be fully understood .
RESULTS : In this study , the transcriptional and metabolic profiles of V-treated Mycobacterium .
bovis BCG were analyzed by RNA-sequencing and LC-MS ( Liquid chromatography coupled to mass spectrometry ) .
The selection of BCG strain was based on its common physiological features shared with @ @ @ @ @ @ @ growth assays demonstrated that Vinhibited the BCG growth rate in vitro .
Transcriptomic analysis revealed that the expression levels of genes related to fatty acid metabolism , cholesterol metabolism , glycolipid catabolism , DNA replication , protein translation , cell division and cell wall formation were significantly downregulated in M. bovis BCG treated with VIn addition , the metabolomics LC-MS data indicated that most of the amino acids and adenosine diphosphate ( ADP ) were decreased in M. bovis BCG strain after Vtreatment .
CONCLUSIONS : This study provides the molecular and metabolic @ @ @ @ @ @ @ M.bovis BCG .

BACKGROUND: Vitamin B(V) is a crucial dietary nutrient and essential cofactor for several key enzymes in the regulation of cellular and metabolic processes, and more importantly in the activation of immune system. To date, the precise role of Vin Mycobacterium tuberculosis remains to be fully understood.
RESULTS: In this study, the transcriptional and metabolic profiles of V-treated Mycobacterium. bovis BCG were analyzed by RNA-sequencing and LC-MS (Liquid chromatography coupled to mass spectrometry). The selection of BCG strain was based on its common physiological features shared with M. tuberculosis. The results of cell growth assays demonstrated that Vinhibited the BCG growth rate in vitro. Transcriptomic analysis revealed that the expression levels of genes related to fatty acid metabolism, cholesterol metabolism, glycolipid catabolism, DNA replication, protein translation, cell division and cell wall formation were significantly downregulated in M. bovis BCG treated with VIn addition, the metabolomics LC-MS data indicated that most of the amino acids and adenosine diphosphate (ADP) were decreased in M. bovis BCG strain after Vtreatment.
CONCLUSIONS: This study provides the molecular and metabolic bases to understand the impacts of Von M.bovis BCG.


greenmedinfo--2020-04-17--Diversity of energy metabolism in immune responses regulated by microorganisms and dietary nutrition

Diversity of energy metabolism in immune responses regulated by microorganisms and dietary nutrition.

Immune metabolism has been recognized as a new paradigm in the regulation of host immunity .
In the environment , @ @ @ @ @ pathogenic and non-pathogenic and/or beneficial ones .
Immune cells exhibit various responses against different types @ @ @ @ @ to be associated with changes in energy metabolism .
In addition , dietary nutrition influences @ @ @ @ @ by immune cells .
In this review , we describe the complex network of immune @ @ @ @ @ nutrition , microorganisms and host immunity for the control of immunologic health and diseases .

Immune metabolism has been recognized as a new paradigm in the regulation of host immunity. In the environment, there are many microorganisms including pathogenic and non-pathogenic and/or beneficial ones. Immune cells exhibit various responses against different types of microbes, which seem to be associated with changes in energy metabolism. In addition, dietary nutrition influences host metabolism and consequent responses by immune cells. In this review, we describe the complex network of immune metabolism from the perspectives of nutrition, microorganisms and host immunity for the control of immunologic health and diseases.


greenmedinfo--2020-04-17--Prevalence of low plasma vitamin B1 in the stroke population admitted to acute inpatient rehabilitat

Prevalence of low plasma vitamin B1 in the stroke population admitted to acute inpatient rehabilitation.

OBJECTIVE : To determine the prevalence of vitamin B1 ( VitB1 ) deficiency in the stroke population admitted to acute @ @ @ @ @ 119 consecutive stroke patients admitted to stroke service from 1 January 2018 to 31 December @ @ @ @ @ were 17 patients ( 14 % ; 95 % CI 9-22 % ) with low @ @ @ @ @ 2-3 nmol/L , an additional 58 ( 49 % ; CI 40-58 % ) patients @ @ @ @ @ a range of 4-9 nmol/L , twenty-five patients ( 21 % ; CI 15-29 % @ @ @ @ @ with a range of 10-15 nmol/L , and nineteen patients ( 16 % ; CI @ @ @ @ @ VitB1 with a range of 16-43 nmol/L .
CONCLUSIONS : In this cohort of patients @ @ @ @ @ at an acute rehabilitation facility , there is evidence of thiamine deficiency .
Moreover , @ @ @ @ @ is inadequate acute intake of VitB1 .
Given the role of thiamine deficiency in neurologic @ @ @ @ @ the role of thiamine optimization in the acute stroke rehabilitation population is warranted .

OBJECTIVE: To determine the prevalence of vitamin B1 (VitB1) deficiency in the stroke population admitted to acute inpatient rehabilitation.
DESIGN: Retrospective cohort study.
SETTING: Acute inpatient rehabilitation facility at an academic medical center.
PARTICIPANTS: 119 consecutive stroke patients admitted to stroke service from 1 January 2018 to 31 December 2018.
INTERVENTIONS: Not applicable.
MAIN OUTCOME MEASURES: Plasma VitB1 level.
RESULTS: There were 17 patients (14%; 95% CI 9-22%) with low VitB1 with a range of 2-3 nmol/L, an additional 58 (49%; CI 40-58%) patients had normal low VitB1 with a range of 4-9 nmol/L, twenty-five patients (21%; CI 15-29%) had normal high VitB1 with a range of 10-15 nmol/L, and nineteen patients (16%; CI 10-24%) had high VitB1 with a range of 16-43 nmol/L.
CONCLUSIONS: In this cohort of patients admitted to the stroke service at an acute rehabilitation facility, there is evidence of thiamine deficiency. Moreover, the data suggest that there is inadequate acute intake of VitB1. Given the role of thiamine deficiency in neurologic function, further study of the role of thiamine optimization in the acute stroke rehabilitation population is warranted.


greenmedinfo--2020-04-17--Prevalence of Vitamin-D deficiency is related to severity of liver damage in Hepatitis-C patients.

Objective : Serum Vitamin-D plays pivotal role in inflammatory and infectious diseases ; among them liver infections are more distinct .
This study was aimed to determine Vitamin-D status in HCV-infected patients and healthy controls in Faisalabad , Pakistan .
Methods : We performed randomized cross-sectional study of 74 individuals from 20August , 2017 to 20February 2018 at The University of Faisalabad and Dar us Shifa Clinic , Faisalabad .
Fifty-one patients were hepatitis C RNA-PCR positive ( 22 compensated cirrhotic and 29 decompensated cirrhotic patients ) .
In addition , 23 subjects without liver disease were recruited as healthy @ @ @ @ @ @ @ ARTUS® HCV QS-RGQ V1 .
Vitamin-D levels were measured by chemiluminescence .
SPSS version 20 was used for statistical analysis .
Results : The mean level of Vitamin-D was significantly lower in HCV patients in compensated and decompensated cirrhotic patients ( 26.85 ng/mL & 20.65 ng/mL respectively ) as compared to healthy controls ( 30.41 ng/mL ) .
This study showed sub optimal level of Vitamin-D in 76.5 % of HCV patients .
Vitamin-D insufficiency ( 21-29 ng/mL ) as prevalent among healthy individuals ( 47.8 % ) as well as in HCV @ @ @ @ @ @ @ < 0.001 ) .
In addition , Vitamin-D levels showed inverse relationship with more severe conditions of liver disease as 55.2 % of decompensated cirrhosis patients were sufferer of Vitamin-D deficiency as compared to 13.6 % deficiency of Vitamin-D in compensated cirrhotic group ( P < 0.0001 ) .
Conclusion : Suboptimal levels of Vitamin-D ( deficiency or insufficiency ) are prevalent in patients having hepatitis C infection as compared to healthy controls .
Deficiency of Vitamin-D was directly associated with severity of disease .

Objective: Serum Vitamin-D plays pivotal role in inflammatory and infectious diseases; among them liver infections are more distinct. This study was aimed to determine Vitamin-D status in HCV-infected patients and healthy controls in Faisalabad, Pakistan.
Methods: We performed randomized cross-sectional study of 74 individuals from 20August, 2017 to 20February 2018 at The University of Faisalabad and Dar us Shifa Clinic, Faisalabad. Fifty-one patients were hepatitis C RNA-PCR positive (22 compensated cirrhotic and 29 decompensated cirrhotic patients). In addition, 23 subjects without liver disease were recruited as healthy control. HCV RNA-PCR was performed by ARTUS® HCV QS-RGQ V1. Vitamin-D levels were measured by chemiluminescence. SPSS version 20 was used for statistical analysis.
Results: The mean level of Vitamin-D was significantly lower in HCV patients in compensated and decompensated cirrhotic patients (26.85 ng/mL&20.65 ng/mL respectively) as compared to healthy controls (30.41 ng/mL). This study showed sub optimal level of Vitamin-D in 76.5% of HCV patients. Vitamin-D insufficiency (21-29 ng/mL) as prevalent among healthy individuals (47.8%) as well as in HCV patients (39.2%) (P<0.001). In addition, Vitamin-D levels showed inverse relationship with more severe conditions of liver disease as 55.2% of decompensated cirrhosis patients were sufferer of Vitamin-D deficiency as compared to 13.6% deficiency of Vitamin-D in compensated cirrhotic group (P<0.0001).
Conclusion: Suboptimal levels of Vitamin-D (deficiency or insufficiency) are prevalent in patients having hepatitis C infection as compared to healthy controls. Deficiency of Vitamin-D was directly associated with severity of disease.


greenmedinfo--2020-04-17--Vitamin D deficiency and autism spectrum disorder.

Vitamin D is a neurosteroid hormone crucially involved in neurodevelopment .
Neural cell proliferation , neurotransmission , oxydative stress and immune function , represent the main mechanisms mediated by vitamin D in the Central Nervous System .
Therefore , its deficiency during pregnancy and early childhood may significantly impact on a developing brain , leading to possible adverse neuropsychological outcomes including Autism Spectrum Disorder ( ASD ) .
Significant vitamin D deficiency is described within children affected by ASD and in pregnant mothers whose offspring will later develop ASD , suggesting a possible role of the hormone as a contributing @ @ @ @ @ @ @ .
We reviewed the actual literature on the potential contributing role of prenatal and early postnatal vitamin D deficiency in ASD etiopathogenesis , at both genetic and environmental level , and the possible effect of vitamin D supplementation in autistic children .
Conflicting but promising results emerged on the topic .
Further Randomized Controlled Trials studies carried out during pregnancy and early infancy are necessary for better understanding the possible contribution of vitamin D deficiency in the etiopathogenesis of autism and the potential efficacy of the hormone supplementation on the improvement of ASD @ @ @

Vitamin D is a neurosteroid hormone crucially involved in neurodevelopment. Neural cell proliferation, neurotransmission, oxydative stress and immune function, represent the main mechanisms mediated by vitamin D in the Central Nervous System. Therefore, its deficiency during pregnancy and early childhood may significantly impact on a developing brain, leading to possible adverse neuropsychological outcomes including Autism Spectrum Disorder (ASD). Significant vitamin D deficiency is described within children affected by ASD and in pregnant mothers whose offspring will later develop ASD, suggesting a possible role of the hormone as a contributing risk factor in the etiopathogenesis of ASD. We reviewed the actual literature on the potential contributing role of prenatal and early postnatal vitamin D deficiency in ASD etiopathogenesis, at both genetic and environmental level, and the possible effect of vitamin D supplementation in autistic children. Conflicting but promising results emerged on the topic. Further Randomized Controlled Trials studies carried out during pregnancy and early infancy are necessary for better understanding the possible contribution of vitamin D deficiency in the etiopathogenesis of autism and the potential efficacy of the hormone supplementation on the improvement of ASD core symptoms.


greenmedinfo--2020-04-18--Vitamin D rescues impaired Mycobacterium tuberculosis-mediated tumor necrosis factor release in macr

Vitamin D rescues impaired Mycobacterium tuberculosis-mediated tumor necrosis factor release in macrophages of HIV-seropositive individuals.

Mycobacterium tuberculosis disease represents an enormous global health problem , with exceptionally high morbidity and mortality in HIV-seropositive ( HIV ( + ) ) persons .
Alveolar macrophages from HIV ( + ) persons demonstrate specific and targeted impairment of critical host cell responses , including impaired M. tuberculosis-mediated tumor necrosis factor ( TNF ) release and macrophage apoptosis .
Vitamin D may promote anti-M. tuberculosis responses through upregulation of macrophage NO , NADPH oxidase , cathelicidin , and autophagy mechanisms , but whether vitamin D promotes anti-M. tuberculosis mechanisms in HIV ( + ) macrophages is not known .
@ @ @ @ @ @ @ exposed to M. tuberculosis demonstrated robust release of TNF , IκB degradation , and NF-κB nuclear translocation , and these responses were independent of vitamin D pretreatment .
In marked contrast , HIV ( + ) U1 human macrophages exposed to M. tuberculosis demonstrated very low TNF release and no significant IκB degradation or NF-κB nuclear translocation , whereasvitamin D pretreatment restored these critical responses .
The vitamin D-mediated restored responses were dependent in part on macrophage CD14 expression .
Importantly , similar response patterns were observed with clinically relevant human alveolar macrophages @ @ @ @ @ @ @ + ) persons at high clinical risk of M. tuberculosis infection .
Taken together with the observation that local bronchoalveolar lavage fluid ( BALF ) levels of vitamin D are severely deficient in HIV ( + ) persons , the data from this study demonstrate that exogenous vitamin D can selectively rescue impaired critical innate immune responses in vitro in alveolar macrophages from HIV ( + ) persons at risk for M. tuberculosis disease , supporting a potential role for exogenous vitamin D as a therapeutic adjuvant in M. tuberculosis infection in HIV @ @ @ @ @

Mycobacterium tuberculosis disease represents an enormous global health problem, with exceptionally high morbidity and mortality in HIV-seropositive (HIV(+)) persons. Alveolar macrophages from HIV(+) persons demonstrate specific and targeted impairment of critical host cell responses, including impaired M. tuberculosis-mediated tumor necrosis factor (TNF) release and macrophage apoptosis. Vitamin D may promote anti-M. tuberculosis responses through upregulation of macrophage NO, NADPH oxidase, cathelicidin, and autophagy mechanisms, but whether vitamin D promotes anti-M. tuberculosis mechanisms in HIV(+) macrophages is not known. In the current study, human macrophages exposed to M. tuberculosis demonstrated robust release of TNF, IκB degradation, and NF-κB nuclear translocation, and these responses were independent of vitamin D pretreatment. In marked contrast, HIV(+) U1 human macrophages exposed to M. tuberculosis demonstrated very low TNF release and no significant IκB degradation or NF-κB nuclear translocation, whereasvitamin D pretreatment restored these critical responses. The vitamin D-mediated restored responses were dependent in part on macrophage CD14 expression. Importantly, similar response patterns were observed with clinically relevant human alveolar macrophages from healthy individuals and asymptomatic HIV(+) persons at high clinical risk of M. tuberculosis infection. Taken together with the observation that local bronchoalveolar lavage fluid (BALF) levels of vitamin D are severely deficient in HIV(+) persons, the data from this study demonstrate that exogenous vitamin D can selectively rescue impaired critical innate immune responses in vitro in alveolar macrophages from HIV(+) persons at risk for M. tuberculosis disease, supporting a potential role for exogenous vitamin D as a therapeutic adjuvant in M. tuberculosis infection in HIV(+) persons.


greenmedinfo--2020-04-18--Vitamin D supplementation promotes immune recovery.

Introduction : much evidence confirms that vitamin D may be associated with an improvement in CD4 cell counts in HIV-infected individuals , where antiretroviral therapy ( ART ) is used and associated with decreased 25 ( OH ) D levels .
Objective : to carry out a systematic review on the effect of vitamin D supplementation on HIV-infected adult patients .
Methods : the research was conducted in the databases Science Direct , PubMed , BVS , Scielo Cochrane and Periods , from February to April 2018 , with publication limit from 2000 to 2018 , without restriction of gender @ @ @ @ @ @ @ older than 18 years .
To evaluate the quality of the studies , we used the protocol Preferred Reporting Items for Systematic Reviews and Meta-Analyzes ( PRISMA ) and the Jadad scale .
Results : the search initially resulted in 198 articles .
After the selection process 5 articles were identified as eligible , where they highlight that vitamin D supplementation may be an associated and effective intervention to reduce hypovitaminosis .
ART reduces vitamin D3 levels and changes its metabolism , being associated with the risk of mortality .
However , adequate @ @ @ @ @ @ @ are positively associated with the number of CD4 + cells and the reduction of infection levels .
Conclusion : vitamin D supplementation promotes immune recovery .
However , the cases analysed were few , insufficient to fully confirm the benefits and recommend supplementation .
Therefore , intervention studies are needed to elucidate the role of vitamin D in human protection against HIV infections .

Introduction: much evidence confirms that vitamin D may be associated with an improvement in CD4 cell counts in HIV-infected individuals, where antiretroviral therapy (ART) is used and associated with decreased 25(OH)D levels. Objective: to carry out a systematic review on the effect of vitamin D supplementation on HIV-infected adult patients. Methods: the research was conducted in the databases Science Direct, PubMed, BVS, Scielo Cochrane and Periods, from February to April 2018, with publication limit from 2000 to 2018, without restriction of gender, ethnicity and involving individuals with age older than 18 years. To evaluate the quality of the studies, we used the protocol Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) and the Jadad scale. Results: the search initially resulted in 198 articles. After the selection process 5 articles were identified as eligible, where they highlight that vitamin D supplementation may be an associated and effective intervention to reduce hypovitaminosis. ART reduces vitamin D3 levels and changes its metabolism, being associated with the risk of mortality. However, adequate levels of 25(OH)D are positively associated with the number of CD4 + cells and the reduction of infection levels. Conclusion: vitamin D supplementation promotes immune recovery. However, the cases analysed were few, insufficient to fully confirm the benefits and recommend supplementation. Therefore, intervention studies are needed to elucidate the role of vitamin D in human protection against HIV infections.


greenmedinfo--2020-04-18--Vitamin D deficiency is associated with tuberculosis infection among household contacts in Ulaanbaat

Vitamin D deficiency is associated with tuberculosis infection among household contacts in Ulaanbaatar, Mongolia.

Vitamin D deficiency ( VDD ) is a known risk factor for tuberculous infection .
We investigated if VDD is a risk factor for tuberculous infection among the household contacts ( HHCs ) of patients with tuberculosis ( TB ) in Mongolia.All HHCs of TB patients diagnosed in Khan-Uul District , Mongolia , were enrolled .
The serum level of 25-hydroxyvitamin D [ 25 ( OH ) D ] was detected and TB infection determined using QuantiFERON-TB Gold Plus ( QFT-Plus ) .
A tuberculin skin test ( TST ) reading > 10 mm was considered to be positive .
@ @ @ @ @ @ @ routine surveillance of the National Tuberculosis Programme.Among study participants , 48.2 % ( 135/285 ) were QFT-Plus-positive .
Of QFT-positive HHCs , 77.0 % ( 104/135 ) were TST-positive and the overall concordance of tests was low ( κ 0.374 , < 0.001 ) .
A low serum level of 25 ( OH ) D was an independent predictor for QFT-Plus positivity ( < 0.001 ) .
CD8T-cell stimulation measured by QFT-Plus had borderline association with the serum level of 25 ( OH ) D ( = 0.089 ) .We showed a high @ @ @ @ @ @ @ Mongolia .
QFT-Plus could decrease the number of people requiring TB preventive treatment , in addition to aiding detection of new TB infection .
A low serum level of vitamin D was an independent predictor of TB infection , but not a predictor of stimulation of CD8T cells .

Vitamin D deficiency (VDD) is a known risk factor for tuberculous infection. We investigated if VDD is a risk factor for tuberculous infection among the household contacts (HHCs) of patients with tuberculosis (TB) in Mongolia.All HHCs of TB patients diagnosed in Khan-Uul District, Mongolia, were enrolled. The serum level of 25-hydroxyvitamin D [25(OH)D] was detected and TB infection determined using QuantiFERON-TB Gold Plus (QFT-Plus). A tuberculin skin test (TST) reading>10 mm was considered to be positive. Epidemiological and bacteriological data were collected from routine surveillance of the National Tuberculosis Programme.Among study participants, 48.2% (135/285) were QFT-Plus-positive. Of QFT-positive HHCs, 77.0% (104/135) were TST-positive and the overall concordance of tests was low (κ 0.374,<0.001). A low serum level of 25(OH)D was an independent predictor for QFT-Plus positivity (<0.001). CD8T-cell stimulation measured by QFT-Plus had borderline association with the serum level of 25(OH)D (= 0.089).We showed a high rate of TB infection among HHCs in Mongolia. QFT-Plus could decrease the number of people requiring TB preventive treatment, in addition to aiding detection of new TB infection. A low serum level of vitamin D was an independent predictor of TB infection, but not a predictor of stimulation of CD8T cells.


greenmedinfo--2020-04-18--Severe vitamin d deficiency is a latent tuberculosis infection risk factor.

To examine the potential association between vitamin D ( VitD ) deficiency and latent tuberculosis infection ( LTBI ) and its effect on TB infection conversion ( TBIC ) incidence.We carried out a cross-sectional and prospective cohort study of nine pulmonary TB cases that occurred in 2015-2016 in five nursing homes and one mental disability institution in Castellon , Spain .
QuantiFERON-TB Gold and the tuberculin skin test were used to detect LTBI and TBIC , respectively .
Serum 25-hydroxyvitamin D was measured using chemiluminescence immunoassay .
Poisson regression and inverse probability weighting were used for statistical analyses.The study included @ @ @ @ @ @ @ 48 relatives of TB cases ( participation rate 82 % ) : of these , respectively 122 ( 27.2 % ) , 37 ( 10.9 % ) and 7 ( 14.6 % ) were LTBI-positive ; and respectively 22 ( 7.7 % ) , 10 ( 3.8 % ) and 1 ( 3.7 % ) were TBIC-positive .
LTBI was not associated with VitD status .
Severe VitD deficiency ( SVDD ; defined as VitD level < 10 ng/ml ) , found in 45.1 % of residents , as well as VitD levels @ @ @ @ @ @ @ 95 % CI 1.48-73.26 ) , were associated with increased TBIC risk ( adjusted relative risk [ aRR ] 12.1 , 95 % CI 1.51-97.10 ) , suggesting SVDD as a threshold effect.Severe VitD deficiency is a TBIC risk factor .

To examine the potential association between vitamin D (VitD) deficiency and latent tuberculosis infection (LTBI) and its effect on TB infection conversion (TBIC) incidence.We carried out a cross-sectional and prospective cohort study of nine pulmonary TB cases that occurred in 2015-2016 in five nursing homes and one mental disability institution in Castellon, Spain. QuantiFERON-TB Gold and the tuberculin skin test were used to detect LTBI and TBIC, respectively. Serum 25-hydroxyvitamin D was measured using chemiluminescence immunoassay. Poisson regression and inverse probability weighting were used for statistical analyses.The study included 448 residents, 341 staff members with 48 relatives of TB cases (participation rate 82%): of these, respectively 122 (27.2%), 37 (10.9%) and 7 (14.6%) were LTBI-positive; and respectively 22 (7.7%), 10 (3.8%) and 1 (3.7%) were TBIC-positive. LTBI was not associated with VitD status. Severe VitD deficiency (SVDD; defined as VitD level<10 ng/ml), found in 45.1% of residents, as well as VitD levels of<30 ng/ml (aRR 10.41 95% CI 1.48-73.26), were associated with increased TBIC risk (adjusted relative risk [aRR] 12.1, 95% CI 1.51-97.10), suggesting SVDD as a threshold effect.Severe VitD deficiency is a TBIC risk factor.


greenmedinfo--2020-04-18--Vitamin D level and it is association with the severity of pulmonary tuberculosis in patients.

Globally , tuberculosis is one of the major causes of morbidity and mortality in many countries .
Previous studies suggest that the incidence and severity of tuberculosis are associated with low levels of vitamin D ( Vit D ) .
Therefore , this study aimed to determine the occurrence and associated factors of vitamin D3 deficiency in pulmonary tuberculosis patients at White Nile State , Sudan .
101 individuals of diagnosed pulmonary tuberculosis patients ( 71 males and 30 females ) and 100 non-TB controls ( 58 males and 42 females ) were included in this study .
Sputum samples @ @ @ @ @ @ @ to examination for acid-fast bacilli ( AFB ) using Ziehl-Neelsen ( ZN ) stain and Gene Xpert analysis .
Blood samples were collected from both groups and Serum 25 ( OH ) -vitamin D3 was determined by an Enzyme-Linked Immunosorbent Assay .
HIV infection in Tuberculosis ( TB ) group was also investigated using the immunochromatographic test .
In our study , the majority of TB patients were suffered from TB relapse ( 36.6 % ) ; non-HIV infected individuals ( 99.1 % ) or showed a positive result for AFB ( 61.4 @ @ @ @ @ @ @ Moreover , there is a significant difference in microscopy findings and bacillary levels of AFB , and Rifampicin ( RIF ) susceptibility pattern ofstrain among sputum samples of TB patients , P-values less 0.0001 .
Furthermore , we found that TB patients were suffered from vitamin D deficiency .
In particular , the mean of vitamin D level was significantly much lower in TB patients ( 26.7± 1.6 ) compared to non-TB controls ( 117.3 ± 3.2 ) , P-value equal 0.0001 .
Likewise , it 's much lower in females , individuals @ @ @ @ @ @ @ with high bacillary levels or those infected by Rifampicin resistance strain .
Accordingly , our study was highlighted the TB and Vit D deficiency relationship and showed the need for further studies to a better understanding of the impact of TB on Vit D level and investigate whether vitamin D supplementation can have a role in the prevention and treatment of tuberculosis .

Globally, tuberculosis is one of the major causes of morbidity and mortality in many countries. Previous studies suggest that the incidence and severity of tuberculosis are associated with low levels of vitamin D (Vit D). Therefore, this study aimed to determine the occurrence and associated factors of vitamin D3 deficiency in pulmonary tuberculosis patients at White Nile State, Sudan. 101 individuals of diagnosed pulmonary tuberculosis patients (71 males and 30 females) and 100 non-TB controls (58 males and 42 females) were included in this study. Sputum samples were obtained from TB patients and subjected to examination for acid-fast bacilli (AFB) using Ziehl-Neelsen (ZN) stain and Gene Xpert analysis. Blood samples were collected from both groups and Serum 25(OH)-vitamin D3 was determined by an Enzyme-Linked Immunosorbent Assay. HIV infection in Tuberculosis (TB) group was also investigated using the immunochromatographic test. In our study, the majority of TB patients were suffered from TB relapse (36.6%); non-HIV infected individuals (99.1%) or showed a positive result for AFB (61.4%) in Gene Xpert analysis. Moreover, there is a significant difference in microscopy findings and bacillary levels of AFB, and Rifampicin (RIF) susceptibility pattern ofstrain among sputum samples of TB patients, P-values less 0.0001. Furthermore, we found that TB patients were suffered from vitamin D deficiency. In particular, the mean of vitamin D level was significantly much lower in TB patients (26.7± 1.6) compared to non-TB controls (117.3 ± 3.2), P-value equal 0.0001. Likewise, it's much lower in females, individuals of 21-40 years old, and patients with high bacillary levels or those infected by Rifampicin resistance strain. Accordingly, our study was highlighted the TB and Vit D deficiency relationship and showed the need for further studies to a better understanding of the impact of TB on Vit D level and investigate whether vitamin D supplementation can have a role in the prevention and treatment of tuberculosis.


greenmedinfo--2020-04-18--Vitamin D treatment of peripheral blood mononuclear cells modulated immune activation and reduced su

Vitamin D treatment of peripheral blood mononuclear cells modulated immune activation and reduced susceptibility to HIV-1 infection of CD4+ T lymphocytes.

INTRODUCTION : Mucosal immune activation , in the context of sexual transmission of HIV-1 infection , is crucial , as the increased presence of activated T cells enhance susceptibility to infection .
In this regard , it has been proposed that immunomodulatory compounds capable of modulating immune activation , such as Vitamin D ( VitD ) may reduce HIV-1 transmission and might be used as a safe and cost-effective strategy for prevention .
Considering this , we examined the in vitro effect of the treatment of peripheral blood mononuclear cells ( PBMCs ) with the active form of VitD , @ @ @ @ @ @ @ and susceptibility of CD4+ T cells to HIV-1 infection .
METHODS : We treated PBMCs from healthy HIV unexposed individuals ( Co-HC ) and frequently exposed , HIV-1 seronegative individuals ( HESNs ) from Colombia and from healthy non-exposed individuals from Canada ( Ca-HC ) with calcitriol and performed in vitro HIV-1 infection assays using X4- and R5-tropic HIV-1 strains respectively .
In addition , we evaluated the activation and function of T cells and the expression of viral co-receptors , and select antiviral genes following calcitriol treatment .
RESULTS : Calcitriol reduced @ @ @ @ @ @ @ and the number of viral particles per cell , for both , X4- and R5-tropic viruses tested in the Co-HC and the Ca-HC , respectively , but not in HESNs .
Furthermore , in the Co-HC , calcitriol reduced the frequency of polyclonally activated T cells expressing the activation markers HLA-DR and CD38 , and those HLA-DR+CD38- , whereas increased the subpopulation HLA-DR-CD38+ .
Calcitriol treatment also decreased production of granzyme , IL-2 and MIP-1β by T cells and increased the transcriptional expression of the inhibitor of NF-kB and the antiviral genes cathelicidin @ @ @ @ @ @ @ from Co-HC .
CONCLUSION : Our in vitro findings suggest that VitD treatment could reduce HIV-1 transmission through a specific modulation of the activation levels and function of T cells , and the production of antiviral factors .
In conclusion , VitD remains as an interesting potential strategy to prevent HIV-1 transmission that should be further explored .

INTRODUCTION: Mucosal immune activation, in the context of sexual transmission of HIV-1 infection, is crucial, as the increased presence of activated T cells enhance susceptibility to infection. In this regard, it has been proposed that immunomodulatory compounds capable of modulating immune activation, such as Vitamin D (VitD) may reduce HIV-1 transmission and might be used as a safe and cost-effective strategy for prevention. Considering this, we examined the in vitro effect of the treatment of peripheral blood mononuclear cells (PBMCs) with the active form of VitD, calcitriol, on cellular activation, function and susceptibility of CD4+ T cells to HIV-1 infection.
METHODS: We treated PBMCs from healthy HIV unexposed individuals (Co-HC) and frequently exposed, HIV-1 seronegative individuals (HESNs) from Colombia and from healthy non-exposed individuals from Canada (Ca-HC) with calcitriol and performed in vitro HIV-1 infection assays using X4- and R5-tropic HIV-1 strains respectively. In addition, we evaluated the activation and function of T cells and the expression of viral co-receptors, and select antiviral genes following calcitriol treatment.
RESULTS: Calcitriol reduced the frequency of infected CD4+ T cells and the number of viral particles per cell, for both, X4- and R5-tropic viruses tested in the Co-HC and the Ca-HC, respectively, but not in HESNs. Furthermore, in the Co-HC, calcitriol reduced the frequency of polyclonally activated T cells expressing the activation markers HLA-DR and CD38, and those HLA-DR+CD38-, whereas increased the subpopulation HLA-DR-CD38+. Calcitriol treatment also decreased production of granzyme, IL-2 and MIP-1β by T cells and increased the transcriptional expression of the inhibitor of NF-kB and the antiviral genes cathelicidin (CAMP) and APOBEC3G in PBMCs from Co-HC.
CONCLUSION: Our in vitro findings suggest that VitD treatment could reduce HIV-1 transmission through a specific modulation of the activation levels and function of T cells, and the production of antiviral factors. In conclusion, VitD remains as an interesting potential strategy to prevent HIV-1 transmission that should be further explored.


greenmedinfo--2020-04-18--Vitamin D enhances responses to interferon-β in Multiple sclerosis.

OBJECTIVE : To determine the effect of vitamin D3 on interferon-β ( IFN-β ) response and immune regulation in MS mononuclear cells ( MNCs ) .
METHODS : MNCs from 126 subjects , including therapy-naive patients with different forms of MS , plus patients with MS receiving IFN-β or glatiramer treatment , plus healthy controls were incubated in vitro with IFN-β-1b ± vitamin D3 ( calcitriol ) .
Activation of the IFN-β-induced transcription factor , p-Y-STAT1 , and antiviral myxovirus A ( MxA ) protein was measured with flow cytometry and Western blots ; serum proteins were measured with a @ @ @ @ @ @ @ Vitamin D enhanced in vitro IFN responses , as measured by induction of p-Y-STAT1 and MxA in MNCs , T cells , and monocytes .
Vitamin D augmentation of IFN responses was seen in untreated and in IFN-β-1b-treated MS .
The combination of vitamin D plus IFN-β reduced Th1 and Th17 cytokines , and increased Th2 responses , reversing the effect of IFN-β alone .
Exacerbations and progression in untreated patients reduced the vitamin D enhancement of IFN responses .
Vitamin D had less effect on IFN response in clinically stable glatiramer-treated than @ @ @ @ @ @ @ D enhances IFN-β induction of multiple proteins and also reverses the Th1/Th2 bias in MS seen with IFN-β alone .
The combination of vitamin D and IFN-β has potential benefit in ameliorating MS .

OBJECTIVE: To determine the effect of vitamin D3 on interferon-β (IFN-β) response and immune regulation in MS mononuclear cells (MNCs).
METHODS: MNCs from 126 subjects, including therapy-naive patients with different forms of MS, plus patients with MS receiving IFN-β or glatiramer treatment, plus healthy controls were incubated in vitro with IFN-β-1b ± vitamin D3 (calcitriol). Activation of the IFN-β-induced transcription factor, p-Y-STAT1, and antiviral myxovirus A (MxA) protein was measured with flow cytometry and Western blots; serum proteins were measured with a customized 31-protein multiplex assay.
RESULTS: Vitamin D enhanced in vitro IFN responses, as measured by induction of p-Y-STAT1 and MxA in MNCs, T cells, and monocytes. Vitamin D augmentation of IFN responses was seen in untreated and in IFN-β-1b-treated MS. The combination of vitamin D plus IFN-β reduced Th1 and Th17 cytokines, and increased Th2 responses, reversing the effect of IFN-β alone. Exacerbations and progression in untreated patients reduced the vitamin D enhancement of IFN responses. Vitamin D had less effect on IFN response in clinically stable glatiramer-treated than in IFN-β-treated patients.
CONCLUSION: Vitamin D enhances IFN-β induction of multiple proteins and also reverses the Th1/Th2 bias in MS seen with IFN-β alone. The combination of vitamin D and IFN-β has potential benefit in ameliorating MS.


greenmedinfo--2020-04-18--Calcitriol reinforced the sensitivity of papillary thyroid carcinoma cells to doxorubicin.

There is increasing evidence that vitamin D deficiency is the risk factor for multiple diseases , such as immune disorder @ @ @ @ @ .
Calcitriol is the active form of vitamin D with beneficial effects on anti-cancer by @ @ @ @ @ VDR ) .
The primary aim of this study was to investigate the role of @ @ @ @ @ ( PTC ) and explore the possible mechanism .
We found nuclear VDR expression in @ @ @ @ @ with STAT3 hyperphosphorylation that indicated worse PTC clinicopathologic characteristics .
Calcitriol treatment up-regulated VDR and @ @ @ @ @ ( PTPN2 ) expression , down-regulated signal transducers and activators of transcription ( STAT3 ) @ @ @ @ @ drug Doxorubicin-induced apoptosis in PTC cell lines .
However , the apoptosis-promoting effect of Calcitriol @ @ @ @ @ by STAT3 hyperphosphorylation , indicating suppression of STAT3 phosphorylation was essential for combined treatment of @ @ @ @ @ .
Together , these results suggested that Calcitriol reinforced the sensitivity of PTC cells to @ @ @ @ @ pathway .

There is increasing evidence that vitamin D deficiency is the risk factor for multiple diseases, such as immune disorder, cardiovascular disease and cancer. Calcitriol is the active form of vitamin D with beneficial effects on anti-cancer by binding vitamin D receptor (VDR). The primary aim of this study was to investigate the role of Calcitriol on papillary thyroid carcinoma (PTC) and explore the possible mechanism. We found nuclear VDR expression in PTC samples was negatively correlated with STAT3 hyperphosphorylation that indicated worse PTC clinicopathologic characteristics. Calcitriol treatment up-regulated VDR and protein tyrosine phosphatase N 2 (PTPN2) expression, down-regulated signal transducers and activators of transcription (STAT3) phosphorylation and thereby facilitating chemotherapy drug Doxorubicin-induced apoptosis in PTC cell lines. However, the apoptosis-promoting effect of Calcitriol and Doxorubicin co-treatment was abrogated by STAT3 hyperphosphorylation, indicating suppression of STAT3 phosphorylation was essential for combined treatment of Calcitriol and Doxorubicin in PTC. Together, these results suggested that Calcitriol reinforced the sensitivity of PTC cells to Doxorubicin by regulating VDR/PTPN2/p-STAT3 signalling pathway.