Helicobacter pylori infection as a model for gastrointestinal immunity and chronic inflammatory diseases.
Approximately 50% of humanity is infected with Helicobacter pylori. It is a life-long infection that elicits a marked host inflammatory response; however, natural infection fails to yield protective immunity. Rather than providing protection, the chronic inflammatory response associated with natural infection contributes to tissue damage and the pathogenesis of gastroduodenal disease, including atrophic gastritis, peptic ulcer, and gastric cancer. While bacterial factors are important triggers of inflammation, many subjects infected with strains bearing putative virulence factors remain free from disease. Recent genetic studies have implicated the host's immune and inflammatory responses, suggesting that disease results from an interaction between bacterial and environmental factors in genetically susceptible hosts. Other digestive diseases, including celiac disease and inflammatory bowel disease, mimic this paradigm, where it appears that luminal triggers only manifest disease in subjects with the right combination of host and environmental factors. Since infection with H. pylori is relatively common, it is possible to study the impact of a specific etiologic agent on the pathogenesis of disease in humans. This approach has illuminated the complexity of the pathogenic mechanisms, but the advances achieved to date may provide some hints regarding the pathogenesis of chronic inflammatory diseases elsewhere in the digestive tract.
Ernst
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PB
Gastroenterology and Hepatology Division, Department of Internal Medicine, University of Virginia, Charlottesville, VA 22908, USA. pernst@virginia.edu
Takaishi
H
H
Crowe
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SE
D002908:Chronic Disease; D005767:Gastrointestinal Diseases / Q000276:immunology* / Q000503:physiopathology*; D016481:Helicobacter Infections / Q000276:immunology* / Q000473:pathology*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D007249:Inflammation; D015212:Inflammatory Bowel Diseases / Q000276:immunology* / Q000503:physiopathology