Innate Immunity of Adipose Tissue in Rodent Models of Local and SystemicStaphylococcus aureusInfection

Abstract

Background. The role of adipose tissue in systemic inflammation during bacterial infection is unclear. Effects ofStaphylococcus aureusinfection on adipocytes in rodent models of experimental endocarditis and peritonitis, the impact ofS. aureusinfection on gene expression in epididymal and subcutaneous adipose tissue, and effects ofS. aureusinfection on the toll-like receptor-2- (TLR2-) cathelicidin pathway in vivo and in vitro were investigated.Material and methods.The rat model of catheter-inducedS. aureusendocarditis and the mouse model ofS. aureus-induced peritonitis were used for infection experiments, gene expression profiling in adipose tissue, and measurement of cytokines. 3T3-L1 adipocytes were analyzed for expression of the TLR2-cathelicidin pathway.Results. Upon systemic bacterial infection byS. aureus, there is a shift from anti- to proinflammatory cytokines in serum and in adipose tissue gene expression. The TLR2-cathelicidin pathway is increasingly expressed during adipocyte differentiation in vitro and is induced upon stimulation by synthetic lipopeptides.Conclusions. Systemic infection by Gram-positive bacteria induces proinflammatory transformation of adipose tissue sites distinct from infection sites, documented on the levels of gene expression and secreted mediators. The TLR2-cathelicidine pathway is expressed and highly inducible in adipocytes in vitro. Lipopeptides are important immune-modulators of adipocytes in both gene expression and protein secretion.