Virulence Factors ofHelicobacter pylori

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Abstract
Helicobacter pylori can be considered a very successful organism effectively colonizing the majority of the world's population. Although various disease states associated with this infection have been described, the mechanisms of pathogenicity remain unknown. The easiest virulence factors to identify are those enabling the organism to colonize the hazardous microenvironment of the gastric epithelium, survive at this site, and multiply sufficiently for transmission to a new host. The factors identified to date include the bacterial enzymes urease and catalase, flagella, and lectin-like adhesins. In addition, it is proposed that the organism has evolved mechanisms to avoid the local antibody responses of the host. Several putative virulence factors that could directly cause gastroduodenal damage have also been identified. These include the direct tissue damage by cytotoxins or the products of urease activity and the indirect tissue damage due to disruption of mucin integrity. Such mechanisms may contribute to peptic ulcer formation; however, the chronic superficial gastritis most frequently associated with this infection is probably caused by immunopathologic events mediated by the host in response to the continued antigen load on the gastric mucosa.