The human gastric colonizer Helicobacter pylori: a challenge for host-parasite glycobiology

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Abstract
The Gram-negative bacterium Helicobacter pylori was first described in 1983 and currently represents one of the most active single research topics in biomedicine. It is specific for the human stomach and chronically colonizes a majority of the global population, which results in a symptom-free local inflammation. In 10–20% of carriers, gastroduodenal disease develops, including gastric or duodenal ulcer, and atrophic gastritis, which is a precondition to gastric cancer. A probable long coevolution of microbe and homo sapiens in a restricted niche has apparently generated a complex and sophisticated interplay. Access to complete bacterial genome sequences assists in a comparative functional characterization. A dynamic glycosylation of both microbe and host cells is of growing interest to analyze. Several glycoforms of bacterial surface lipopolysaccharides show advanced molecular mimicry of host epitopes and a distinct phase variation. An unusually large family of 32 outer membrane proteins probably reflects the complex interrelationship with the host. The unique diversity found for carbohydrate-binding specificities may be mediated by these surface proteins, of which the Lewis b–binding adhesin is the only known example so far, and these binding activities are subject to phase variation. The host mucosa glycosylation may also vary with different conditions, allowing a modulated crosstalk between microbe and host. The bacterium actively stimulates the host inflammatory response, apparently for nutritional purposes, and there is no evidence for a spontaneous elimination of the microbe. Colonization appears to be preventive for upper stomach and esophageal diseases. Current antibiotic treatment eradicates the microbe and cures ulcer disease. Alternative approaches must, however, be developed for a potential global prevention of disease.