REPLICATION OF CHLAMYDIA-PNEUMONIAE IN-VITRO IN HUMAN MACROPHAGES, ENDOTHELIAL-CELLS, AND AORTIC ARTERY SMOOTH-MUSCLE CELLS

Chlamydia pneumoniae has recently been associated with atherosclerotic lesions in coronary arteries. To investigate the biological basis for the dissemination and proliferation of this organism in such lesions, the in vitro growth of C. pneumoniae was studied in two macrophage ce ll lines, peripheral blood monocyte-derived macrophages, human broncho alveolar lavage macrophages, several endothelial cell lines, and aorti c smooth muscle cells. Five strains of C. pneumoniae were capable of t hree passages in human U937 macrophages and in murine RAW 246.7 macrop hages. Titers were suppressed in both macrophage types with each passa ge, as compared with growth titers in HEp-2 cells. Both human bronchoa lveolar lavage macrophages and peripheral blood monocyte derived macro phages were able to inhibit C. pneumoniae after 96 h of growth. Eleven C. pneumoniae strains were capable of replicating in normal human aor tic artery-derived endothelial cells, umbilical vein-derived endotheli al cells, and pulmonary artery endothelial cells. Infection in human a ortic artery smooth muscle cells was also established for 13 strains o f C. pneumoniae. The in vitro ability of C. pneumoniae to maintain inf ections in macrophages, endothelial cells, and aortic smooth muscle ce lls may provide support for the hypothesis that C. pneumoniae can infe ct suck cells and, when infection is followed by an immune response, m ay contribute to atheroma formation in vivo. More studies are needed t o investigate the complex relationship between lytic infection and per sistence and the potential for C. pneumoniae to influence the generati on of atheromatous lesions.