BACKGROUND: Recent findings have established an association between obesity and 
immune dysfunction. However, most of the studies investigating the effects of 
obesity on immune function have been carried out in genetically obese rodent 
models. Since human obesity is mostly due to intake of a high fat diet and 
decreased energy expenditure, we asked whether immunological defects also occur 
in diet-induced obesity. Specifically, we focused on the function of monocytes 
and macrophages, as these cells are thought to be involved in the low-grade 
inflammation present in obesity. METHODS: Male Sprague-Dawley rats were fed a 
high-fat or a standard chow diet for either 2 or 10 weeks. At the end of the 
intervention period animals were anaesthetised, blood collected for 
determination of plasma mediator concentrations and lipopolysaccharide (LPS) 
stimulated production of TNF-alpha by monocytes. LPS stimulated production of 
TNF-alpha in alveolar macrophages was also determined. RESULTS: High-fat feeding 
for either 2 or 10 weeks resulted in significant increases in fat mass and serum 
leptin. Although increased serum leptin has previously been linked to modulation 
of innate immunity, we found no significant difference in the LPS stimulated 
production of TNF-alpha by either blood monocytes or alveolar macrophages 
between the dietary groups. Furthermore, we failed to find a significant 
increase in circulating TNF-alpha concentrations in obese animals, as reported 
for genetically obese animals. CONCLUSION: Our data suggest that defects in 
innate immune function observed in genetically obese animals are not mimicked by 
dietary obesity, and may more likely reflect the gross abnormality in leptin 
function of these models. Further work is required delineate the effects of 
dietary obesity on inflammatory state and immune function.