Growth in vascular cells and cytokine production by Chlamydia pneumoniae

The proposed pathogenesis of Chlamydia pneumoniae in atherosclerosis is sup ported by the finding that C. pneumoniae can initiate and sustain growth in human vascular cells. In vitro growth of C. pneumoniae is found in macroph ages, peripheral blood monocyte (PBMC)-derived macrophages, endothelial cel ls, and aortic artery smooth muscle cells. U-937 macrophages infected with C. pneumoniae are capable of transmitting the infection to human coronary a rtery endothelial cells (CAEC) with direct cellular contact. Production of cytokines by cells infected with C. pneumoniae indicates that the organism can stimulate the immune system. CAEC infected with C. pneumoniae produce m ore interleukin-8 than cells sham inoculated with negative control cells. W hen interferon-gamma is used to stimulate HEp-2 cells, U-937 cells, and PBM C (before infection with C. pneumoniae), inhibition of a productive growth cycle occurs in a dose-related response. Studies are needed to learn the re lationship between productive infection and persistence, the ability of C. pneumoniae to affect the immune response, and the potential for C. pneumoni ae to influence atheromatous lesions.