Chlamydial heat shock protein 60 and lipopolysaccharide: potential virulence determinants in atherogenesis.
Chlamydia pneumoniae infection is associated with atherosclerosis and may be an emerging risk factor in coronary artery disease. C. pneumoniae can infect, multiply within and modulate the function of all atheroma cell types. Specific chlamydial virulence determinants have been identified that permit interaction with host cells and dysregulate cell function. In particular, chlamydial heat shock protein 60 and lipopolysaccharide may modulate cell function to dysregulate lipid metabolism, induce inflammatory cytokine cascades and trigger production of cross-reactive antibodies that initiate and promote atherogenesis. This paper reviews chlamydial heat shock protein 60 and lipopolysaccharide as potential virulence determinants in atherogenesis.
Kalayoglu
Murat V
MV
Department of Ophthalmology-Massachusetts Eye and Ear Infirmary, Harvard Medical School, 243 Charles Street, Boston, MA 02114, USA. mkalayog@hotmail.com
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000276:immunology / Q000503:physiopathology*; D018834:Chaperonin 60 / Q000276:immunology / Q000502:physiology*; D002689:Chlamydia / Q000276:immunology / Q000378:metabolism* / Q000472:pathogenicity* / Q000502:physiology; D002690:Chlamydia Infections / Q000382:microbiology / Q000473:pathology; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology*; D037521:Virulence Factors / Q000276:immunology / Q000502:physiology*
D018834:Chaperonin 60; D008070:Lipopolysaccharides; D037521:Virulence Factors