Bacterial factors and immune pathogenesis in Helicobacter pylori infection
T Shimoyamab, J E Crabtreea
a Molecular
Medicine Unit, Level 7, Clinical Sciences Building, St. James's
University Hospital, Leeds LS9 7TF, UK, b First Department of Internal Medicine, Hirosaki University
School of Medicine, Hirosaki, Japan
Correspondence to: Dr Crabtree.
| The first 150 words of the full text of this article appear below. |
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Summary |
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Virulent Helicobacter pylori strains which have been clinically associated with severe outcome induce increased gastric mucosal immune responses. Although several bacterial pathogenic factors have been shown to have a considerable role in H pylori infection, variability in host immune responses may also contribute to mucosal damage in H pylori associated gastritis.
Since the discovery of H pylori, many studies have
implicated infection with this bacterium in the pathogenesis of gastric and duodenal diseases. However, most patients with H
pylori infection have chronic gastritis only and few develop
peptic ulcers or gastric tumours. To date, the role of bacterial
virulence factors such as vacA, cagA and
lipopolysaccharide (LPS) in the pathogenesis of H pylori
infection has been extensively studied. The host's mucosal immune
response, which includes activation of neutrophils, T cells and
complement, has also been the subject of recent investigation. Both
bacterial and host factors are likely to
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