F Mégraud1. 1. Laboratoire de Bactériologie-Enfants, Hôpital Pellegrin, Bordeaux, France.
Abstract
PURPOSE: To review the various toxic factors produced directly or indirectly by Helicobacter pylori and discuss their relative importance in H. pylori infection. RESULTS: The toxic factors produced by H. pylori can act at different levels. At the epithelial cell level H. pylori enzymes generate toxic molecules: ammonia (urease), lysolecithin (phospholipases) and acetaldehyde (alcohol dehydrogenase). The harmful effects of ammonia have been studied the most intensively and seem to be a likely mechanism of pathogenicity. A vacuolating cytotoxin is expressed in 50-60% of the strains while the gene is present in all. Despite the fact that its potential toxic effect is low, the cytotoxin is associated with ulcer development. Another protein, CagA is a marker for the presence of the toxin. H. pylori can also produce a hemolysin, a platelet-activating factor and a factor that alters parietal cell function. At the mucus level, it does not seem that H. pylori enzymes degrade mucin, and the thinness of the layer could be due to inhibition of mucus exocytosis. CONCLUSION: H. pylori have a wide range of toxic factors which can act together but no one factor is considered sufficient alone to explain the observed lesions.
PURPOSE: To review the various toxic factors produced directly or indirectly by Helicobacter pylori and discuss their relative importance in H. pyloriinfection. RESULTS: The toxic factors produced by H. pylori can act at different levels. At the epithelial cell level H. pylori enzymes generate toxic molecules: ammonia (urease), lysolecithin (phospholipases) and acetaldehyde (alcohol dehydrogenase). The harmful effects of ammonia have been studied the most intensively and seem to be a likely mechanism of pathogenicity. A vacuolating cytotoxin is expressed in 50-60% of the strains while the gene is present in all. Despite the fact that its potential toxic effect is low, the cytotoxin is associated with ulcer development. Another protein, CagA is a marker for the presence of the toxin. H. pylori can also produce a hemolysin, a platelet-activating factor and a factor that alters parietal cell function. At the mucus level, it does not seem that H. pylori enzymes degrade mucin, and the thinness of the layer could be due to inhibition of mucus exocytosis. CONCLUSION:H. pylori have a wide range of toxic factors which can act together but no one factor is considered sufficient alone to explain the observed lesions.