Chlamydia pneumoniae enhances cytokine-stimulated human monocyte matrix metalloproteinases through a prostaglandin E2-dependent mechanism.
Exposure of human monocytes to Chlamydia pneumoniae resulted in a significant enhancement of matrix metalloproteinase (MMP) 1 and 9 production following stimulation with tumor necrosis factor alpha and granulocyte monocyte-colony stimulating factor. The effect of C. pneumoniae on monocyte MMPs was mediated through the induction of prostaglandin E(2). These findings may have implications for atherosclerotic plaque rupture.
Kim
Min P
MP
Immunopathology Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, 30 Convent Dr., Building 30, Room 325, Bethesda, MD 20892-4352, USA.
Gaydos
Charlotte A
CA
Wood
Billie Jo
BJ
Hardick
Justin P
JP
Zhang
Yahong
Y
Wahl
Larry M
LM
D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D003324:Coronary Artery Disease / Q000209:etiology; D015232:Dinoprostone / Q000502:physiology*; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology*; D006801:Humans; D020781:Matrix Metalloproteinase 1 / Q000096:biosynthesis*; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis*; D009000:Monocytes / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D014409:Tumor Necrosis Factor-alpha; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D020780:Matrix Metalloproteinase 9; D020781:Matrix Metalloproteinase 1; D015232:Dinoprostone