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Pathogenesis of H elicobacter pylori Infection
Author(s) -
Delahay Robin M.,
Rugge Massimo
Publication year - 2012
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2012.00976.x
Subject(s) - caga , bacterial adhesin , virulence , helicobacter pylori , biology , pathogenesis , secretion , disease , immunology , microbiology and biotechnology , host (biology) , asymptomatic , population , pathogen , genetics , gene , medicine , biochemistry , environmental health , pathology
Although H elicobacter pylori infection is highly prevalent in the global human population, the majority of infected individuals remain asymptomatic. A complex combination of host, environmental, and bacterial factors are considered to determine susceptibility and severity of outcome in the subset of individuals that develop clinical disease. These factors collectively determine the ability of H . pylori to colonize the gastric mucosa and profoundly influence the nature of the interaction that ensues. Many studies over the last year provide new insight into H . pylori virulence strategies and the activities of critical bacterial determinants that modulate the host environment. These latter include the secreted proteins C ag A and V ac A and adhesins B ab A and O ip A , which directly interact with host tissues. Observations from several studies extend the functional repertoire of C ag A and the cag type IV secretion system in particular, providing further mechanistic understanding of how these important determinants engage and activate host signalling pathways important in the development of disease.