Cellular responses induced after contact with Helicobacter pylori

被引：63

作者：

Censini, S ^{[1
]}

Stein, M ^{[1
]}

Covacci, A ^{[1
]}

机构：

[1] IRIS Chiron SPA, I-53100 Siena, Italy

来源：

CURRENT OPINION IN MICROBIOLOGY | 2001年 / 4卷 / 01期

关键词：

D O I：

10.1016/S1369-5274(00)00162-4

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Contact-dependent activation of the cag organelle, a type IV secretion system of Helicobacter pylori, promotes translocation of CagA into the host cell. CagA is an immunodominant antigen of H. pylori, encoded by cag. It is thought to be associated with severe clinical outcomes, but has an unclear role in pathogenesis. Now we know that CagA is injected into the host and is tyrosine-phosphorylated by a membrane-associated eukaryotic tyrosine kinase. After activation, CagA induces morphological changes in the host, as well as actin reorganization, variations in the cell cycle and autocrine effects. Subversion of cell control may ultimately lead to cellular damage and to increased risks for gastric cancer development. cag instability contributes to long-term persistence within the host by attenuating bacterial virulence. We still do not know if additional factors are co-translocated with CagA and we do not know their specific mechanisms of action, but there is a strong experimental evidence that indicates that cag is the major player in the host-pathogen relationship.

引用

页码：41 / 46

页数：6

共 43 条

[11]

DEIBEL C, 1998, MOL MICROBIOL, V30, P147

[12] Activation of the CDC42 effector N-WASP by the Shigella flexneri IcsA protein promotes actin nucleation by Arp2/3 complex and bacterial actin-based motility [J].