An update on Helicobacter pylori
An update on Helicobacter pylori
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幽门螺杆菌的最新进展
DOI：
10.1097/00001574-199501000-00014
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发表时间：
1995
期刊：
影响因子：
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通讯作者：
T. Wadström
中科院分区：
文献类型：
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作者：
T. Wadström
由于动物模型的局限性和各种体外观察的相关性问题，关于幽门螺杆菌的致病机制仍存在很大争议。与其他细菌病原体一样，幽门螺杆菌的毒力因子可分为三类：定植因子、致病因子和促进持久性因子。定植因素允许病原体在宿主中建立，包括运动性、尿素酶产生和黏附机制。致病因素包括细胞毒素和尿素酶、胃粘膜屏障的破坏、炎性介质的诱导、胃生理改变的产生以及可能的菌株特异性溃疡特性。最后，幽门螺杆菌感染的重要性可能是因为它具有长期存活的能力。幽门螺杆菌感染可以被认为是一个缓慢的适应过程。这种病原体存活并与宿主免疫系统相互作用的机制可能为其他持久性粘膜病原体提供一个模型。根除幽门螺杆菌现在是消化性溃疡的公认治疗方法，并可能导致消除胃恶性肿瘤的一个主要危险因素。
Because of the limitations of animal models and the question of relevance of various in vitro observations, much controversy remains about the pathogenic mechanisms by which Helicobacter pylori can induce disease. Like those of other bacterial pathogens, the putative virulence factors of H. pylori can be divided into three groups: colonization factors, disease-inducing factors, and factors promoting persistence. Colonization factors allow the pathogen to become established in the host and include motility, urease production, and adhesion mechanisms. Disease-inducing factors consist of cytotoxins and urease, disruption of the gastric mucosal barrier, induction of inflammatory mediators, production of changed gastric physiology and possibly strain specific ulcerogenic properties. Finally, the importance of H. pylori infection may be due to its capacity for long-term persistence. An H. pylori infection can be considered a slow adaptive process. The mechanisms by which this pathogen survives and interacts with the host immune system may provide a model for other persistent mucosal pathogens. Eradication of H. pylori is now accepted therapy for peptic ulcer and may lead to elimination of a major risk factor for gastric malignancies.