Author(s): Gaydos CA
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Abstract The proposed pathogenesis of Chlamydia pneumoniae in atherosclerosis is supported by the finding that C. pneumoniae can initiate and sustain growth in human vascular cells. In vitro growth of C. pneumoniae is found in macrophages, peripheral blood monocyte (PBMC)-derived macrophages, endothelial cells, and aortic artery smooth muscle cells. U-937 macrophages infected with C. pneumoniae are capable of transmitting the infection to human coronary artery 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 more interleukin-8 than cells sham inoculated with negative control cells. When interferon-gamma is used to stimulate HEp-2 cells, U-937 cells, and PBMC (before infection with C. pneumoniae), inhibition of a productive growth cycle occurs in a dose-related response. Studies are needed to learn the relationship between productive infection and persistence, the ability of C. pneumoniae to affect the immune response, and the potential for C. pneumoniae to influence atheromatous lesions.
This article was published in J Infect Dis
and referenced in Journal of Multiple Sclerosis