Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Thromb Haemost. 2009 Dec;102(6):1064-70. doi: 10.1160/TH09-06-0348.

Chlamydia pneumoniae adversely modulates vascular cell properties by direct interaction with signalling cascades.

Author information

  • 1Institute of Medical Microbiology, Hygiene and Infectious Diseases, University Hospital Salzburg, Paracelsus Medical Private University, Salzburg, Austria

Abstract

Due to its dependence on intracellular development Chlamydia pneumoniae has developed numerous strategies to create an adequate environment within its host cells ensuring both chlamydial reproduction and target cell survival. The bacterium that has been related to atherogenesis due to its presence in vascular tissue is able to enter a persistent state of chronic infection in the vasculature that escapes antibiotic targeting. Ingestion of the bacterium results in severe modifications and reprogramming of signalling pathways and the metabolism of the host cell. Processes range from the prevention of direct lysosomal destruction of chlamydial inclusions to the inhibition of host cell apoptosis and an enhanced cellular glucose uptake to maintain energy-consuming mechanisms. Furthermore, infection regularly causes the development of a proinflammatory and proproliferative phenotype in the host cell in vitro, ex vivo and in vivo and own new findings suggest a detrimental proliferative loop within vascular cells upon a modified endothelin-1 axis demonstrating a potential for proatherosclerotic processes in early and progressed atherosclerosis. This review displays crucial mechanisms of Chlamydia pneumoniae-induced interactions with vascular host cell signalling cascades with an emphasis on mitogenic and inflammatory processes as well as target cell activation.

PMID:
19967136
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Schattauer Verlag
    Loading ...
    Write to the Help Desk