Signal transduction pathways activated in endothelial cells following infection with Chlamydia pneumoniae

Chlamydia pneumoniae is an important respiratory pathogen, Recently, its pr esence has been demonstrated in atherosclerotic lesions. in this study, we characterized C. pneumoniae-mediated activation of endothelial cells and de monstrated an enhanced expression of endothelial adhesion molecules followe d by subsequent rolling, adhesion, and transmigration of leukocytes (monocy tes, granulocytes). These effects were blocked by mAbs against endothelial and/or leukocyte adhesion molecules (beta(1) and beta(2) integrins). Additi onally, activation of different signal transduction pathways in C. pneumoni ae-infected endothelial cells was shown: protein tyrosine phosphorylation, up-regulation of phosphorylated p42/p44 mitogen-activated protein kinase, a nd NF-kappa B activation/translocation occurred within 10-15 min. Increased mRNA and surface expression of E-selectin, ICAM-1, and VCAM-1 were noted w ithin hours. Thus, C, pneumoniae triggers a cascade of events that could le ad to endothelial activation, inflammation, and thrombosis, which in turn m ay result in or mag promote atherosclerosis.