Premium
Pathogenesis of Helicobacter pylori Infection
Author(s) -
Torres Javier,
Backert Steffen
Publication year - 2008
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.1523-5378.2008.00630.x
Subject(s) - caga , helicobacter pylori , virulence , pathogenicity island , bacterial outer membrane , biology , virulence factor , pathogenesis , signal transduction , microbiology and biotechnology , carcinogenesis , pathogenicity , effector , mechanism (biology) , immunology , cancer , genetics , gene , escherichia coli , philosophy , epistemology
The clinical outcome of Helicobacter pylori infection is determined by a complex scenario of interactions between the bacterium and the host. The main bacterial factors associated with colonization and pathogenicity comprise outer membrane proteins including BabA, SabA, OipA, AlpA/B, as well as the virulence factors CagA in the cag pathogenicity island ( cag PAI) and the vacuolating cytotoxin VacA. The multitude of these proteins and allelic variation 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 the induction of membrane dynamics, actin‐cytoskeletal rearrangements and the disruption of cell‐to‐cell junctions as well as proliferative, pro‐inflammatory and antiapoptotic nuclear responses. An animal model using the Mongolian gerbil is a useful system to study the gastric pathology of H. pylori infection.