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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:789.)
© 2003 American Heart Association, Inc.

Vascular Biology

Recruitment of Chlamydia pneumoniae–Infected Macrophages to the Carotid Artery Wall in Noninfected, Nonatherosclerotic Mice

Andreas E. May; Vanessa Redecke; Sabine Grüner; Roland Schmidt; Steffen Massberg; Thomas Miethke; Birgit Ryba; Clarissa Prazeres da Costa; Albert Schömig; Franz-Josef Neumann

From Deutsches Herzzentrum und 1. Medizinische Klinik (A.E.M., V.R., S.G., R.S., S.M., B.R., A.S.) and Institut für Mikrobiologie, Immunologie und Hygiene (V.R., T.M., C.P.d.C.), Klinikum Rechts der Isar, Technische Universität München and Herz-Zentrum Bad Krozingen (F.-J.N.), Germany.

Correspondence to Andreas E. May, MD, Deutsches Herzzentrum, Technische Universität München, Lazarettstr. 36, D-80636 München, Germany. E-mail may{at}dhm.mhn.de

Objective— Monocyte recruitment into the subendothelium is a crucial step in atherogenesis. Chlamydia pneumoniae resides in circulating monocytes and in the atherosclerotic vascular wall. However, the role of C pneumoniae for monocyte recruitment is unknown. The aim of this study was to examine the impact of C pneumoniae on monocyte adhesion and migration.

Methods and Results— C pneumoniae–infected, fluorescence-labeled mouse macrophages (ANA-1) were injected intravenously into noninfected, healthy mice. In vivo videomicroscopy showed increased rolling and firm adhesion to the carotid artery compared with noninfected macrophages. In vitro, C pneumoniae infection (yielding 25% to 35% infected monocytes) increased adhesion of human monocytes or MonoMac6 cells to human umbilical vein endothelial cells and improved cell migration through endothelial-like ECV604 cells. Cell adhesion was inhibited by antibody blockade of very late antigen-4, lymphocyte function-associated antigen-1, macrophage antigen-1, or urokinase receptor, which were found upregulated or activated on C pneumoniae infection (flow cytometry). In contrast, C trachomatis did not induce monocyte adhesion at comparable infection rates (25% to 35%), indicating a unique activation pathway for C pneumoniae. Polymyxin B did not affect C pneumoniae–induced adhesion, excluding a relevant role of lipopolysaccharide in this process.

Conclusions— These data indicate that C pneumoniae can direct monocytes to predilection sites of nonatherosclerotic vessel walls in vivo by activation of the integrin adhesion receptor system.

Key Words: Chlamydia pneumoniae • monocyte • adhesion • integrin • atherosclerosis

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