title: Toll-like receptor 11 (TLR11) prevents Salmonella penetration into the murine Peyer patches.
abstract: 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.
authors.affiliation: Texas A&M University Health Science Center, Houston, Texas 77030, USA.
authors.forename: Zhongcheng
authors.initials: Z
authors.lastname: Shi
authors.forename: Zhenyu
authors.initials: Z
authors.lastname: Cai
authors.forename: Jingcui
authors.initials: J
authors.lastname: Yu
authors.forename: Tingting
authors.initials: T
authors.lastname: Zhang
authors.forename: Shu
authors.initials: S
authors.lastname: Zhao
authors.forename: Emanuel
authors.initials: E
authors.lastname: Smeds
authors.forename: Qingyuan
authors.initials: Q
authors.lastname: Zhang
authors.forename: Fen
authors.initials: F
authors.lastname: Wang
authors.forename: Changhong
authors.initials: C
authors.lastname: Zhao
authors.forename: Songbin
authors.initials: S
authors.lastname: Fu
authors.forename: Sankar
authors.initials: S
authors.lastname: Ghosh
authors.forename: Dekai
authors.initials: D
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000235:genetics / Q000276:immunology; D018988:Bacterial Translocation / Q000235:genetics / Q000276:immunology*; D001693:Biological Transport, Active / Q000235:genetics / Q000276:immunology; D016466:CHO Cells; D006224:Cricetinae; D003412:Cricetulus; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology; D051379:Mice; D018345:Mice, Knockout; D010581:Peyer's Patches / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D012480:Salmonella Infections / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D012486:Salmonella typhimurium / Q000502:physiology*; D051198:Toll-Like Receptor 5 / Q000235:genetics / Q000378:metabolism; D051193:Toll-Like Receptors / Q000235:genetics / Q000276:immunology*
chemical_list: D000942:Antigens, Bacterial; C482903:Tlr11 protein, mouse; D051198:Toll-Like Receptor 5; D051193:Toll-Like Receptors