Chlamydia pneumoniae stimulates the proliferation of HUVEC through the induction of VEGF by THP-1.

Chlamydia pneumoniae, a gram-negative bacterium, is an important human intracellular pathogen; studies of C. pneumoniae pathogenesis have shown that the organism can infect many cell types associated with both respiratory and vascular sites, including arterial smooth muscle cells, macrophages and vascular endothelium. Recently, the recognition of atherosclerosis as an inflammatory disease in its genesis, progression and ultimate clinical manifestations has created an interesting area of vascular research. We assessed the hypothesis that growth factors from THP-1 macrophages infected with C. pneumoniae are involved in the regulation of cell proliferation in HUVEC. The induction of these factors were dependent on time of infection, as medium harvested 48 h after infection had a greater activity than media harvested at 12 or 24 h after infection. Heat-killed C. pneumoniae produced similar results to those of live bacteria. In addition, conditioned medium filtered sterile from infected macrophages induced the proliferation of HUVEC, thus demonstrating its angiogenic potential. Moreover, pretreatment of macrophages with cytochalasin D, a phagocytosis inhibitor, yielded almost comparable results, suggesting that bacterium cell-attachment is sufficient for VEGF, IL-1beta and IL-8 induction. Further studies are necessary to elucidate the biological role of chlamydial involvement in the complex and mutifactored processes of angiogenesis and possibly contribute to the development of therapeutic strategies.