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Patients with chronic gastritis produced by Helicobacter pylori are at risk of duodenal and gastric ulceration and gastric cancer. The majority of H. pylori-colonized individuals remain asymptomatic, however, and the mechanism of this resistance is not fully understood. A study published in the March issue of Journal of Clinical Investigation shows that genetic differences between strains of Helicobacter pylori influence host inflammatory responses (J Clin Invest 2001, 107:611-620).

Dawn Israel and colleagues examined in a gerbil model the ability of duodenal and gastric ulcer strains of H. pylori isolates to induce differential host responses in vivo or in vitro. Gastric ulcer strain B128 induced more severe gastritis than did duodenal ulcer strain G1.1. DNA hybridization to a whole H. pylori genome microarray identified a large deletion of the cag pathogenicity island in duodenal ulcer strain G1.1. Partial and complete disruption of the cag island in gastric strain B128 attenuated induction of IL-8 in vitro and significantly decreased gastric inflammation in vivo, suggesting that the ability of H. pylori strains to induce epithelial inflammation is dependent on the presence of an intact cag pathogenicity island.

The authors conclude that "Genotypic markers could be developed not only to identify individuals at risk for specific clinical sequelae of infection, but also to permit selective targeting of therapy for disease prevention."

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