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Salmonella ‐induced SipB‐independent cell death requires Toll‐like receptor‐4 signalling via the adapter proteins Tram and Trif
Author(s) -
Cook Pamela,
Tötemeyer Sabine,
Stevenson Catherine,
Fitzgerald Katherine A.,
Yamamoto Masahiro,
Akira Shizuo,
Maskell Duncan J.,
Bryant Clare E.
Publication year - 2007
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2007.02631.x
Subject(s) - trif , salmonella enterica , programmed cell death , toll like receptor , biology , signal transducing adaptor protein , microbiology and biotechnology , salmonella , receptor , signal transduction , apoptosis , innate immune system , bacteria , biochemistry , genetics
Summary 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.