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Infection and Immunity, February 2008, p. 510-514, Vol. 76, No. 2
0019-9567/08/$08.00+0     doi:10.1128/IAI.01267-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Chlamydia pneumoniae Infection Increases Adherence of Mouse Macrophages to Mouse Endothelial Cells In Vitro and to Aortas Ex Vivo

Naohisa Takaoka,^1, Lee Ann Campbell,¹ Amy Lee,¹ Michael E. Rosenfeld,² and Cho-Chou Kuo^1*

Department of Pathobiology and Epidemiology,¹ Department of Pathology, University of Washington, Seattle, Washington²

Received 14 September 2007/ Returned for modification 23 October 2007/ Accepted 26 November 2007

Interactions between monocytes/macrophages and endothelial cells play an important role in the pathogenesis of atherosclerosis, and the adherence of monocytes to the arterial endothelium is one of the early events in atherogenesis. In the present study, peritoneal macrophages harvested from green fluorescent protein (GFP) transgenic mice were used to analyze how Chlamydia pneumoniae infection affects the adherence of GFP-macrophages to mouse endothelial cells in vitro and to the aorta from normolipidemic and hyperlipidemic mice ex vivo. In vitro studies showed that C. pneumoniae-infected GFP-macrophages adhered better than uninfected macrophages to endothelial cells and GFP-macrophages adhered better to infected than uninfected endothelial cells. The ex vivo studies showed that C. pneumoniae-infected macrophages adhered better than uninfected macrophages to aortas from both normolipidemic and hyperlipidemic C57BL/6J mice and apolipoprotein E (ApoE)-deficient mice. In contrast, adherence of C. pneumoniae-infected macrophages to the aortas of intercellular adhesion molecule 1 (ICAM-1) knockout mice was not enhanced, suggesting that ICAM-1 is crucial for activation of the adherence of C. pneumoniae-infected macrophages to the endothelium. In conclusion, the present study defined a homing mechanism by which C. pneumoniae promotes the adherence of mononuclear phagocytes to the endothelium at the site of atherosclerotic lesion formation to promote the progression of atherosclerosis.

Published ahead of print on 10 December 2007.

Editor: S. R. Blanke

Present address: Department of Urology, Hamamatsu University School of Medicine, Hamamatsu 1-20-1, Hamamatsu 431-3192, Japan.