Literature DB >> 17490432

Salmonella-induced SipB-independent cell death requires Toll-like receptor-4 signalling via the adapter proteins Tram and Trif.

Pamela Cook1, Sabine Tötemeyer, Catherine Stevenson, Katherine A Fitzgerald, Masahiro Yamamoto, Shizuo Akira, Duncan J Maskell, Clare E Bryant.   

Abstract

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.

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Year:  2007        PMID: 17490432      PMCID: PMC2266008          DOI: 10.1111/j.1365-2567.2007.02631.x

Source DB:  PubMed          Journal:  Immunology        ISSN: 0019-2805            Impact factor:   7.397


  50 in total

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9.  Macrophage killing is an essential virulence mechanism of Salmonella typhimurium.

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6.  Roles of the crp and sipB genes of Salmonella enterica serovar Typhimurium in protective efficacy and immune responses to vaccination in mice.

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10.  Dynamics of Salmonella infection of macrophages at the single cell level.

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