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幽门螺杆菌感染的发病机制。

Pathogenesis of Helicobacter pylori infection.

机构信息

Centre for Biomolecular Sciences and Nottingham Digestive Diseases Centre, University of Nottingham, Nottingham, UK.

出版信息

Helicobacter. 2012 Sep;17 Suppl 1:9-15. doi: 10.1111/j.1523-5378.2012.00976.x.

Abstract

Although Helicobacter pylori infection is highly prevalent in the global human population, the majority of infected individuals remain asymptomatic. A complex combination of host, environmental, and bacterial factors are considered to determine susceptibility and severity of outcome in the subset of individuals that develop clinical disease. These factors collectively determine the ability of H. pylori to colonize the gastric mucosa and profoundly influence the nature of the interaction that ensues. Many studies over the last year provide new insight into H. pylori virulence strategies and the activities of critical bacterial determinants that modulate the host environment. These latter include the secreted proteins CagA and VacA and adhesins BabA and OipA, which directly interact with host tissues. Observations from several studies extend the functional repertoire of CagA and the cag type IV secretion system in particular, providing further mechanistic understanding of how these important determinants engage and activate host signalling pathways important in the development of disease.

摘要

尽管全球人类人群中幽门螺杆菌感染极为普遍,但大多数感染者仍无症状。宿主、环境和细菌因素的复杂组合被认为决定了在发展为临床疾病的个体亚群中疾病易感性和结局的严重程度。这些因素共同决定了幽门螺杆菌定植胃黏膜的能力,并深刻影响随后发生的相互作用的性质。过去一年中的许多研究为幽门螺杆菌的毒力策略以及调节宿主环境的关键细菌决定因素的活性提供了新的见解。这些决定因素包括与宿主组织直接相互作用的分泌蛋白 CagA 和 VacA 以及黏附素 BabA 和 OipA。来自几项研究的观察结果扩展了 CagA 的功能范围,特别是 cag 型 IV 型分泌系统,从而进一步深入了解这些重要决定因素如何参与并激活在疾病发展中起重要作用的宿主信号通路。

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