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Chapter 27 : Helicobacter pylori: the Role of the Immune Response in Pathogenesis
Category: Immunology; Clinical Microbiology
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The development of disease as a consequence of Helicobacter. Pylori infection is influenced by human genetic differences, virulence factors expressed by the colonizing strain, and environmental factors such as smoking and concurrent infections. The immune response to infection may be affected by each of these. A wide variety of innate host defense mechanisms are chronically induced by H. pylori on the gastric mucosa, including the expression of proinflammatory and antibacterial factors by gastric epithelial cells. Although all H. pylori strains cause ongoing gastric inflammation, the severity of this gastritis differs profoundly between individual infections, and a major driver of this is whether specific virulence factors are expressed by the infecting strain. The most important and best characterized H. pylori virulence determinant is a group of about 30 genes present in some but not all strains, called the cag Pathogenicity Island (PaI). Small cationic antimicrobial peptides of two main groups, defensins and cathelicidins, are secreted as part of the innate immune response to H. pylori. A microarray study on infected rhesus macaques showed that defensin responses are largely dependent on presence of the cag PaI in the colonizing strain. The antibody response to H. pylori is known to contribute to pathogenesis by triggering autoimmunity. A section of the chapter discusses the role of the different subsets of T-cells in H. pylori-mediated disease in detail. A detailed knowledge of the immune mechanisms required for clearance of H. pylori infection is vital for vaccine development.
Patterns of gastritis and their links with disease
Host immune response gene polymorphisms and their associations with disease
H. pylori virulence factors with known effects on the immune response
Association of T-helper subsets with H. pylori induced inflammation, pathology, and colonization