Induction of tissue factor expression and release as microparticles in ECV304 cell line by Chlamydia pneumoniae infection

The association between Chlainvdia pneumoniae (C. pneumoniae) infection and the onset and progression of atherosclerosis has become apparent recently. Moreover, increased expression Of tissue factor (TF) as a result of C. pnetanoniae infection has been previously demonstrated. We have examined the expression of TF on the surface of endothelial cells and the release of TF-containing cell-derived microparticles, over seven days. Additionally, using cells expressing a procoagulantly active EGFP-TF hybrid protein, we examined the kinetics of TF trafficking on the cells and incorporation into shed microparticles. Finally, in an attempt to associate this with the activation of NF kappa B, we used a luciferase reporter to measure the duration of the activation of this transcription factor. TF-containing microparticles were released within 24 h of infection and continued for up to 7 clays. Moreover, the initial release of TF containing microparticles was associated with NF kappa B activation and was suppressed on inclusion of an NF kappa B inhibitor, pyrrolidinedithiocarbamate ammonium. Moreover, persistent dissemination of TF-containing microparticles at later stages of infection was associated with the release of the infective C pneunioniae elementary bodies. The released procoagulant, cellular microparticies are known to be strongly atherogenic and therefore we suggest a mechanism for the involvement of C pneumoniae in the onset and progression of vascular disease. (c) 2006 Elsevier Ireland Ltd. All rights reserved.