NDLI: Toll-like receptor 4 signalling through MyD88 is essential to control Salmonella enterica serovar Typhimurium infection, but not for the initiation of bacterial clearance

Content Provider	PubMed Central
Author	Talbot, Suzanne Tötemeyer, Sabine Yamamoto, Masahiro Akira, Shizuo Hughes, Katherine Gray, David Barr, Tom Mastroeni, Pietro Maskell, Duncan J. Bryant, Clare E.
Abstract	Toll-like receptor-4 (TLR4) is important in protection against lethal Salmonella enterica serovar Typhimurium (S. Typhimurium) infection. Control of the early stages of sublethal S. Typhimurium infection in mice depends on TLR4-dependent activation of macrophages and natural killer (NK) cells to drive an inflammatory response. TLR4 signals through the adapter proteins Mal/MyD88 and TRIF-related adaptor molecule (TRAM)/TIR-domain-containing adaptor-inducing interferon-b (TRIF). In the mouse typhoid model we showed that TLR4 and MyD88, but not Mal or TRIF, are essential for the control of exponential S. Typhimurium growth. TRIF−/− mice have a higher bacterial load in comparison with wild-type mice during a sublethal infection because TRIF is important for bacterial killing during the first day of systemic disease. Minimal pro-inflammatory responses were induced by S. Typhimurium infection of macrophages from TLR4−/−, MyD88−/− and TRIF−/− mice in vitro. Pro-inflammatory responses from Mal−/− macrophages were similar to those from wild-type cells. The pro-inflammatory responses of TRIF−/− macrophages were partially restored by the addition of interferon-γ (IFN-γ), and TRIF−/− mice produced markedly enhanced IFN-γ levels, in comparison to wild-type mice, probably explaining why bacterial growth can be controlled in these mice. TLR4−/−, MyD88−/−, TRIF−/− and Mal−/− mice all initiated clearance of S. Typhimurium, suggesting that TLR4 signalling is not important in driving bacterial clearance in comparison to its critical role in controlling early bacterial growth in mouse typhoid.
Related Links	http://dx.doi.org/10.1111/j.1365-2567.2009.03146.x
Ending Page	483
Page Count	12
Starting Page	472
File Format	PDF
ISSN	00192805
e-ISSN	13652567
Journal	Immunology
Issue Number	4
Volume Number	128
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2009-12-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Immunology Immunology and Allergy Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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