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Get Free AccessSummary Salmonella enterica serovar typhimurium ( S . typhimurium ) is an intracellular pathogen that causes macrophage cell death by at least two different mechanisms. Rapid cell death is dependent on the Salmonella pathogenicity island‐1 protein SipB whereas delayed cell death is independent of SipB and occurs 18–24 hr post infection. Lipopolysaccharide (LPS) is essential for the delayed cell death. LPS is the main structural component of the outer membrane of Gram‐negative bacteria and is recognized by Toll‐like receptor 4, signalling via the adapter proteins Mal, MyD88, Tram and Trif. Here we show that S . typhimurium induces SipB‐independent cell death through Toll‐like receptor 4 signalling via the adapter proteins Tram and Trif. In contrast to wild type bone marrow derived macrophages (BMDM), Tram –/– and Trif –/– BMDM proliferate in response to Salmonella infection.
Pamela Cook, Sabine Tötemeyer, Catherine Stevenson, Katherine A. Fitzgerald, Masahiro Yamamoto, Akira Shizuo, Duncan J. Maskell, Clare Bryant (2007). <i>Salmonella</i>‐induced SipB‐independent cell death requires Toll‐like receptor‐4 signalling via the adapter proteins Tram and Trif. Immunology, 122(2), pp. 222-229, DOI: 10.1111/j.1365-2567.2007.02631.x.
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Type
Article
Year
2007
Authors
8
Datasets
0
Total Files
0
Language
English
Journal
Immunology
DOI
10.1111/j.1365-2567.2007.02631.x
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