It is well established that CD4CD25 regulatory T cells (Tregs) downregulate 
inflammatory immune responses and help to maintain immune homeostasis. Recent 
reports have shown that ligation of germline encoded pattern recognition 
receptors such as Toll-like receptors can stimulate Tregs and therefore 
implicate Tregs in the pathophysiology of sepsis and other inflammatory 
diseases. In this report, we show that injection of lipopolysaccharide (LPS) 
leads to expansion of CD4CD25FoxP3 Tregs, suggesting that these cells may play 
an important role in immune regulation in LPS-induced acute inflammation. 
Indeed, genetic or immunological inhibition of Treg function using mice lacking 
functional Tregs (CD25 KO mice) or anti-CD25 monoclonal antibody (anti-CD25 
mAb), respectively, led to acute death in an otherwise nonlethal LPS challenge. 
This was accompanied by exaggerated production of proinflammatory cytokines. 
Strikingly, adoptive transfer of CD4CD25 Tregs to CD25 KO mice before LPS 
challenge rescues mice from death. Unlike LPS, depletion of Tregs followed by 
concanavalin A (Con A) challenge does not result in mortality, suggesting that 
Treg depletion does not globally influence all models of acute inflammation. We 
authenticate our findings by showing that depletion of Tregs leads to mortality 
in a nonlethal Escherichia coli challenge accompanied by elevated serum levels 
of proinflammatory cytokines. Collectively, our results indicate that in 
addition to regulation of LPS-induced acute inflammation, Tregs help to improve 
bacterial clearance and promote survival in an acute model of bacterial 
infection.