AN UPDATE ON HELICOBACTER-PYLORI

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.