期刊
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY
卷 55, 期 2, 页码 131-139出版社
WILEY
DOI: 10.1111/j.1574-695X.2008.00514.x
关键词
Chlamydia pneumoniae; atherosclerosis; signal transduction; angiogenesis; inflammation
资金
- Austrian Federal Ministry of Science and Research/GEN-AU
- ERA-Net PathoGenoMics
- Fonds zur Forderung der Wissenschaften, Vienna, Austria [FWF I126-B09]
- Deutsche Forschungsgemeinschaft, Bonn, Germany [DFG Ma 2070/4-3]
Since its description in 1986, Chlamydia pneumoniae has remained one of the most enigmatic pathogens. This intracellular bacterium is highly seroprevalent, but rarely recovered from cell culture, it can genetically switch between a proliferative and a nonreplicative state and has been linked to a vast number of chronic diseases, most notably to atherosclerosis, as it can be found in the plaques. It has become quite clear that persistent bacteria in atherosclerotic lesions cannot be eradicated by currently available antibiotic treatments and that attempts to do so without a better understanding of the pathobiology of chlamydial persistence are futile. However, there is growing knowledge on how vascular chlamydial infection may lead to the pathological reprogramming of the host cell signaling pathways. Chlamydia pneumoniae is now well known to induce, at least in vitro, the two pathogenetic main events that define atherosclerosis: angiogenesis and inflammation. In vivo a contribution of chlamydial infection to the progression of atherosclerosis remains unproven. This minireview provides a brief overview on the proproliferative and proinflammatory effects of vascular C. pneumoniae infection and their potential link to atherogenesis.
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