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

被引：18

作者：

Cook, Pamela

Toetemeyer, Sabine

Stevenson, Catherine

Fitzgerald, Katherine A.

Yamamoto, Masahiro

Akira, Shizuo

Maskell, Duncan J.

Bryant, Clare E.

机构：

[1] Univ Cambridge, Dept Vet Med, Ctr Vet Sci, Cambridge CB3 0ES, England

[2] Univ Massachusetts, Sch Med, Div Infect Dis & Immunol, Worcester, MA USA

[3] Osaka Univ, Inst Microbial Dis, Dept Host Def, Osaka, Japan

来源：

IMMUNOLOGY | 2007年 / 122卷 / 02期

关键词：

monocyte/macrophages; bacterial infection; Toll-like receptor; cell death;

D O I：

10.1111/j.1365-2567.2007.02631.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：222 / 229

页数：8

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[1] The apoptotic signaling pathway activated by Toll-like receptor-2 [J].