Format

Send to

Choose Destination
See comment in PubMed Commons below
Cell Microbiol. 2008 Aug;10(8):1573-81. doi: 10.1111/j.1462-5822.2008.01156.x. Epub 2008 Apr 8.

Role of type IV secretion in Helicobacter pylori pathogenesis.

Author information

  • 1Otto-von-Guericke-Universität Magdeburg, Institut für Medizinische Mikrobiologie, Leipziger Strasse 44, D-39120 Magdeburg, Germany. steffen.backert@med.ovgu.de

Abstract

Helicobacter pylori is a highly successful human-specific gastric pathogen that colonizes more than half the world's population. Infection with this bacterium can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and even cancer. Virulent H. pylori isolates harbour the cag (cytotoxin-associated genes) pathogenicity island, a 40 kb stretch of DNA that encodes components of a type IV secretion system (T4SS). This T4SS forms a pilus for the injection of virulence factors into host target cells such as the CagA oncoprotein. This is accomplished by a specialized adhesin of the pilus surface, the CagL protein, which binds to and activates host cell integrins for subsequent delivery of CagA across the host cell membrane. Injected CagA becomes tyrosine-phosphorylated by Src and Abl family kinases and mimics a host cell protein in binding and activation of multiple signalling factors. Here we review the recent advances in the characterization of phosphorylation-dependent and phosphorylation-independent signalling activities of CagA and the T4SS which include the induction of membrane dynamics, actin cytoskeletal rearrangements and the disruption of cell-to-cell junctions as well as proliferative, pro-inflammatory and anti-apoptotic nuclear responses. The contribution of these signalling cascades to H. pylori pathogenesis is discussed.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Write to the Help Desk