Helicobacter pylori and peptic ulcer disease
Helicobacter pylori, a human specific gastric pathogen, first isolated in 1982 (Lancet, 1273, 1983) has emerged as the causative agent in chronic active gastritis and peptic ulcer disease (Emerging Infectious Diseases 1, 79 1995). In developing countries, the majority of the population is infected already in early childhood, whereas in the industrialized world, less than 20 % of young people are infected, increasing to about half the population by 50 years of age. However, infection prevalence is still very significant because of the medical impact of H. pylori-associated disease. About 10% of people in Sweden develop peptic ulcer sometime during the lifetime. Once an established infection, the bacteria can persist for the lifetime of the host. Interestingly, most infected individuals show no clinical symptoms, implying the influence of additional factors in the pathogenesis of the disease such as the infecting strain. The chronic infection has been correlated to the development of gastric cancer, one of the most common forms of cancer in humans and H. pylori was recently defined a class 1 carcinogen (Lancet, 344, 1078 1994). H. pylori colonizes the human gastric mucosa by adherence to the stomach lining. These adherence properties protect the bacteria from the extreme acidity of the gastric lumen and displacement from the stomach by forces such as gastric emptying. Central to current thinking in pathogenesis is the importance of adherence for colonization and disease.
Fig1. Histo section of H. pylori infected human stomach cells. Bacteria (the orange stained small dots in the center) are seen directly adhering to the surface mucous epithelial cells.
The bacterial binding sites (receptors) in the stomach
Bacteria express adhesion molecules that recognize specific carbohydrates on the stomach cell surface. We have demonstrated the fucosylated blood group antigen Lewis b and H to mediate adherence of H. pylori to human gastric epithelial cells in situ (T. Borén et al. Science 262, 1892 1993). The fucosylated blood group antigens H-1 and Le b are typically found on erythrocytes where they define the O phenotype in the ABO blood group system, but they are also expressed on the epithelial cell surfaces in the stomach.
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Research & Development 
