Helicobacter pylori infection as a model for gastrointestinal immunity andchronic inflammatory diseases

Approximately 50% of humanity is infected with Helicobacter pylori. It is a life-long infection that elicits a marked host inflammatory response; howe ver, natural infection fails to yield protective immunity. Rather than prov iding protection, the chronic inflammatory response associated with natural infection contributes to tissue damage and the pathogenesis of gastroduode nal disease, including atrophic gastritis, peptic ulcer, and gastric cancer . While bacterial factors are important triggers of inflammation, many subj ects infected with strains bearing putative virulence factors remain free f rom disease. Recent genetic studies have implicated the host's immune and i nflammatory responses, suggesting that disease results from an interaction between bacterial and environmental factors in genetically susceptible host s. Other digestive diseases, including celiac disease and inflammatory bowe l disease, mimic this paradigm, where it appears that luminal triggers only manifest disease in subjects with the right combination of host and enviro nmental factors. Since infection with H. pylori is relatively common, it is possible to study the impact of a specific etiologic agent on the pathogen esis of disease in humans. This approach has illuminated the complexity of the pathogenic mechanisms, but the advances achieved to date may provide so me hints regarding the pathogenesis of chronic inflammatory diseases elsewh ere in the digestive tract. Copyright (C) 2001 S. Karger AG, Basel.