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由IV型分泌介导的幽门螺杆菌与宿主细胞的相互作用

Helicobacter pylori-host cell interactions mediated by type IV secretion.

作者信息

Bourzac Kevin M, Guillemin Karen

机构信息

Institute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.

出版信息

Cell Microbiol. 2005 Jul;7(7):911-9. doi: 10.1111/j.1462-5822.2005.00541.x.

Abstract

Helicobacter pylori is a human-specific gastric pathogen that colonizes over half the world's population. Infection with this bacterium is associated with a spectrum of gastric pathologies ranging from mild gastritis to peptic ulcers and gastric cancer. A strong predictor of severe disease outcome is infection with a bacterial strain harbouring the cag (cytotoxin associated gene) pathogenicity island (PAI), a 40 kb stretch of DNA that encodes homologues of several components of a type IV secretion system (TFSS). One gene within the cag PAI, cagA, has been shown to encode a substrate for the TFSS which is translocated into host cells and causes multiple changes in host cell signalling. Here we review recent advances in the characterization of type IV secretion, the activities of CagA and CagA-independent effects of the TFSS, which are contributing to our understanding of H. pylori pathogenesis.

摘要

幽门螺杆菌是一种专性感染人类胃部的病原体,全球半数以上人口都受到其感染。感染这种细菌与一系列胃部疾病相关,范围从轻度胃炎到消化性溃疡及胃癌。严重疾病转归的一个有力预测指标是感染携带细胞毒素相关基因(cag)致病岛(PAI)的菌株,该致病岛是一段40 kb的DNA片段,编码IV型分泌系统(TFSS)若干组分的同源物。cag致病岛内的一个基因cagA已被证明可编码TFSS的一种底物,该底物被转运至宿主细胞内并引起宿主细胞信号传导的多种变化。在此,我们综述IV型分泌特征、CagA活性以及TFSS不依赖CagA的效应等方面的最新进展,这些进展有助于我们理解幽门螺杆菌的致病机制。

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