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Infection and Immunity, June 1999, p. 2909-2915, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Chlamydia pneumoniae Infection of Human Endothelial Cells Induces Proliferation of Smooth Muscle Cells via an Endothelial Cell-Derived Soluble Factor(s)

Brian K. Coombes,1,* and James B. Mahony1,2

Regional Virology and Chlamydiology Laboratory1 and Department of Pathology and Molecular Medicine,2 McMaster University, Hamilton, Ontario, Canada L8N 4A6

Received 22 February 1999/Returned for modification 17 March 1999/Accepted 26 March 1999

An association of Chlamydia pneumoniae with atherosclerosis and coronary heart disease has been determined epidemiologically and by the detection of C. pneumoniae organisms in atherosclerotic lesions in both humans and animal models of atherosclerosis. Previously, it has been shown that C. pneumoniae is capable of replicating in cell types found within atheromatous lesions, viz., endothelial cells, smooth muscle cells (SMC), and macrophages, yet the role of C. pneumoniae in the pathogenesis of atherosclerosis has not been determined. Since intimal thickening is a hallmark of atherosclerosis, we investigated whether C. pneumoniae infection of human umbilical vein endothelial cells (HUVEC) could induce the expression of a soluble factor(s) with mitogenic potential for SMC by using [3H]thymidine incorporation and direct cell counting. Conditioned medium harvested from HUVEC infected with C. pneumoniae stimulated SMC replication in a time- and dose-dependent fashion. Infection studies using various multiplicities of infection (MOIs) ranging from 0.001 to 1 demonstrated a dose-dependent production of the soluble factor(s). At an MOI of 1, SMC stimulation indices were 8.4 (P < 0.01) and 12.2 (P < 0.01) for conditioned media harvested at 24 and 48 h, respectively. To determine whether viable C. pneumoniae was required for production of the soluble factor(s), HUVEC were infected with heat-inactivated C. pneumoniae or with viable organisms in the presence of chloramphenicol. Both treatments produced stimulation indices similar to those for live C. pneumoniae in the absence of chloramphenicol (P > 0.05), indicating that the factor(s) was produced by HUVEC and not by C. pneumoniae and that signal transduction events following chlamydia endocytosis may be important in the production of a soluble factor(s). The ability of C. pneumoniae to elicit an endothelial cell-derived soluble factor(s) that stimulates SMC proliferation may be important in the pathogenesis of atherosclerosis.

* Corresponding author. Mailing address: Regional Virology and Chlamydiology Laboratory, St. Joseph's Hospital, 50 Charlton Ave. E., Hamilton, Ontario, Canada L8N 4A6. Phone: 905-521-6021. Fax: 905-521-6083. E-mail: coombebk{at}fhs.mcmaster.ca.

Infection and Immunity, June 1999, p. 2909-2915, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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