It is indispensable to thoroughly characterize each animal model in order to 
distinguish between primary and secondary effects of genetic changes. The 
present study analyzed Nod1 and Nod2 double deficient (Nod1/2 DKO) mice under 
physiological and inflammatory conditions. Nod1 and Nod2 are members of the 
Nucleotide-binding domain and Leucine-rich repeat containing Receptor (NLR) 
family. Several inflammatory disorders, such as Crohn's disease and asthma, are 
linked to genetic changes in either Nod1 or Nod2. These associations suggest 
that Nod1 and Nod2 play important roles in regulating the immune 
system.Three-month-old wildtype (Wt) and Nod1/2 DKO mice were sacrificed, body 
and organ weight were determined, and blood was drawn. Except for lower liver 
weight in Nod1/2 DKO mice, no differences were found in body/organ weight 
between both strains. Leukocyte count and composition was comparable. No 
significant changes in analyzed plasma biochemical markers were found. 
Additionally, intestinal and vascular permeability was determined. Nod1/2 DKO 
mice show increased susceptibility for intestinal permeability while vascular 
permeability was not affected. Next we induced septic shock and organ damage by 
administering LPS+PGN intraperitoneally to Wt and Nod1/2 DKO mice and sacrificed 
animals after 2 and 24 hours. The systemic inflammatory and metabolic response 
was comparable between both strains. However, renal response was different as 
indicated by partly preserved kidney function and tubular epithelial cell damage 
in Nod1/2 DKO at 24 hours. Remarkably, renal inflammatory mediators Tnfα, KC and 
Il-10 were significantly increased in Nod1/2 DKO compared with Wt mice at 
2 hours.Systematic analysis of Nod1/2 DKO mice revealed a possible role of 
Nod1/2 in the development of renal disease during systemic inflammation.