Chlamydia pneumoniae-infected monocytes exhibit increased adherence to human aortic endothelial cells

Interactions between monocytes and endothelial cells play an important role in the pathogenesis of atherosclerosis, and monocyte adhesion to arterial endothelium is one of the earliest events in atherogenesis. Work presented in this study examined human monocyte adherence to primary human aortic end othelial cells following monocyte infection with Chlamydia pneumoniae, an i ntracellular pathogen associated with atherosclerosis by a variety of sero- epidemiological, pathological and functional studies. Infected monocytes ex hibited enhanced adhesion to aortic endothelial cells in a time- and dose-d ependent manner. Pre-treatment of C. pneumoniae with heat did not effect th e organism's capacity to enhance monocyte adhesion, suggesting that heat-st able chlamydial antigens such as chlamydial lipopolysaccharide (cLPS) media ted monocyte adherence. Indeed, treatment of monocytes with cLPS was suffic ient to increase monocyte adherence to endothelial cells, and increased adh erence of infected or cLPS-treated monocytes could be inhibited by the LPS antagonist lipid X. Moreover, C, pneumoniae-induced adherence could be inhi bited by incubating monocytes with a mAb specific to the human beta2-integr in chain, suggesting that enhanced adherence resulted from increased expres sion of these adhesion molecules. These data show that C. pneumoniae can en hance the capacity of monocytes to adhere to primary human aortic endotheli al cells. The enhanced adherence exhibited by infected monocytes may increa se monocyte residence time in vascular sites with reduced wall shear stress and promote entry of infected cells into lesion-prone locations. (C) 2001 Editions scientifiques et medicales Elsevier SAS.