Toll-like receptors (TLRs) are key molecular sensors used by the mammalian 
innate immune system to detect microorganisms. Although TLR functions in colonic 
immune homeostasis and tolerance to commensal bacteria have been intensively 
researched, the precise roles of different TLRs in response to pathogen 
infection in the gut remain elusive. Peyer patches are the major entrance of 
Salmonella infection and antigen transportation in intestine. Here, we report 
that, in contrast to TLR5 as a "carrier of Salmonella," TLR11 works as a 
"blocker of Salmonella" to prevent highly invasive Salmonella from penetrating 
into the murine Peyer patches and spreading systemically. TLR11 plays an 
important role in mediating TNF-α induction and systemic inflammation in 
response to Salmonella infection. Remarkably, in mice lacking TLR11, apparent 
hemorrhages at Peyer patches are induced by highly invasive Salmonella, a 
phenotype resembling human Salmonella infection. Therefore, our results indicate 
a potentially important role for TLR11 in preventing murine intestinal infection 
and modulating antigen transportation in the gut and imply an important role for 
various TLRs in cooperation with tight control of pathogens penetrating into 
Peyer patches. The TLR11 knock-out mouse can serve as a good animal model to 
study Salmonella infection.