The Vi-capsule prevents Toll-like receptor 4 recognition of Salmonella |
| |
Authors: | Wilson R Paul Raffatellu Manuela Chessa Daniela Winter Sebastian E Tükel Cagla Bäumler Andreas J |
| |
Affiliation: | Department of Medical Microbiology and Immunology, School of Medicine, University of California at Davis, One Shields Ave., Davis, CA, USA. |
| |
Abstract: | The viaB locus enables Salmonella enterica serotype Typhi to reduce Toll-like receptor (TLR) dependent cytokine production in tissue culture models. This DNA region contains genes involved in the regulation ( tviA ), biosynthesis ( tviBCDE ) and export ( vexABCDE ) of the Vi capsule. Expression of the Vi capsule in S. Typhimurium, but not expression of the TviA regulatory protein, reduced tumour necrosis factor-alpha (TNF-α) and IL-6 production by murine bone-marrow derived macrophages. Production of TNF-α and IL-6 was dependent on expression of TLR4 as stimulation of macrophages from TLR4−/− mice with S. Typhimurium did not result in expression of these cytokines. Intraperitoneal infection of mice with S. Typhimurium induced expression of TNF-α and inducible nitric oxide synthase (iNOS) in the liver. Introduction of the cloned viaB region into S. Typhimurium reduced TNF-α and iNOS expression to levels observed after infection with a S. Typhimurium msbB mutant. In contrast, no differences in TNF-α expression between the S. Typhimurium wild type and strains expressing the Vi-capsule or carrying a mutation in msbB were observed after infection of TLR4−/− mice. We conclude that the Vi capsule prevents both in vitro and in vivo recognition of S. Typhimurium lipopolysaccharide by TLR4. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|