Infection with the obligate intracellular bacterial pathogen Chlamydia pneumoniae is emerging as a risk factor in cardiovascular diseases. Evidence supporting a role for C. pneumoniae in atherosclerosis comes from epidemiologybased, pathology-based, cell-culture, and animal model studies, as well as from several clinical trials. Specific chlamydial virulence determinants, most notably chlamydial lipopolysaccharide (cLPS) and chlamydial heat shock protein 60 (cHsp60), have been identified and may contribute to atherogenesis by either serving as antigens or through directly activating key cell types to induce inflammatory cascades. This short review serves to update the reader on new data implicating cHsp60 and other putative chlamydial components in atherogenesis.
Keywords: chlamydia pneumoniae, virulence, lipopolysaccharide, heat shock protein 60, atherosclerosis, inflammation
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