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Pathogenesis of Helicobacter pylori Infection
Author(s) -
Maeda Shin,
Mentis Andreas F.
Publication year - 2007
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.1523-5378.2007.00529.x
Subject(s) - caga , virulence , helicobacter pylori , virulence factor , biology , bacterial outer membrane , microbiology and biotechnology , pathogenicity island , pathogenesis , carcinogenesis , signal transduction , apoptosis , immunology , cancer , genetics , gene , escherichia coli
The clinical outcome of Helicobacter pylori infection is determined by a complex interaction between the bacterium and the host. The main bacterial factors associated with pathogenicity comprise outer membrane proteins, including BabA, SabA, OipA, AlpA, and AlpB, the vacuolating cytotoxin VacA and the products of cag PAI. The multitude of putative virulence factors makes it extremely difficult to test the contribution of each individual factor. Much effort has been put into identifying the mechanism associated with H. pylori ‐associated carcinogenesis. Interaction between bacterial factors such as CagA and host signal transduction pathways seems to be critical for mediating cell transformation, cell proliferation, invasion, apoptosis/anti‐apoptosis, and angiogenesis. An animal model using the Mongolian gerbil is a useful model for showing gastric pathology due to H. pylori infection which is similar to that in humans and can be used to evaluate virulence factors including CagA, host responses, and environmental factors such as salt intake.