Chlamydia pneumoniae facilitates monocyte adhesion to endothelial and smooth muscle cells

Chlamydia pneumoniae has been linked to atherosclerotic heart disease. Howe ver, there is a limited knowledge by which C. pneumoniae gain access to ath eromatous lesions. The adhesion of C. pneumoniae-infected circulatory compo nent(s) to endothelium and smooth muscle cells represents the first step in an inflammatory response. We examined the ability of viable as well as hea t inactivated C. pneumoniae to infect human monocytes and subsequently the ability of infected monocytes to adhere to human coronary artery endothelia l cells (HCAEC) and human coronary smooth muscle cells (HCSMC). Our results demonstrate susceptibility of monocytes to in vitro chlamydial infection. Inclusions of varying sizes and intensities were observed 3-5 days after in oculation with viable C, pneumoniae. Monocytes infected with heat inactivat ed organisms revealed no inclusions, in keeping with the observations of un infected monocytes. Moreover, monocytes infected with viable C. pneumoniae adhered preferentially to HCAEC and HCSMC, as compared to uninfected monocy tes or monocytes harbouring heat inactivated Chlamydia. (C) 2001 Academic P ress.