The Journal of Experimental Medicine
StemCell Technologies
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Published online 7 August 2006 doi:10.1084/jem.20060245
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 9, 2073-2083
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ARTICLE

 Low-grade chronic inflammation in regions of the normal mouse arterial intima predisposed to atherosclerosis

Jenny Jongstra-Bilen1,2, Mehran Haidari1,3, Su-Ning Zhu1,3, Mian Chen1,3, Daipayan Guha1, and Myron I. Cybulsky1,3

1 Toronto General Research Institute, University Health Network, Toronto, Ontario M5G 2C4, Canada
2 Department of Immunology and 3 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada

CORRESPONDENCE Myron Cybulsky: myron.cybulsky{at}utoronto.ca

Atherosclerotic lesions develop in regions of arterial curvature and branch points, which are exposed to disturbed blood flow and have unique gene expression patterns. The cellular and molecular basis for atherosclerosis susceptibility in these regions is not completely understood. In the intima of atherosclerosis-predisposed regions of the wild-type C57BL/6 mouse aorta, we quantified increased expression of several proinflammatory genes that have been implicated in atherogenesis, including vascular cell adhesion molecule–1 (VCAM-1) and a relative abundance of dendritic cells, but only occasional T cells. In contrast, very few intimal leukocytes were detected in regions resistant to atherosclerosis; however, abundant macrophages, including T cells, were found throughout the adventitia (Adv). Considerably lower numbers of intimal CD68+ leukocytes were found in inbred atherosclerosis-resistant C3H and BALB/c mouse strains relative to C57BL/6 and 129; however, leukocyte distribution throughout the Adv of all strains was similar. The predominant mechanism for the accumulation of intimal CD68+ cells was continued recruitment of bone marrow–derived blood monocytes, suggestive of low-grade chronic inflammation. Local proliferation of intimal leukocytes was low. Intimal CD68+ leukocytes were reduced in VCAM-1–deficient mice, suggesting that mechanisms of leukocyte accumulation in the intima of normal aorta are analogous to those in atherosclerosis.

Abbreviations used: Adv, adventitia; ANOVA, analysis of variance; DT, descending thoracic aorta; GC and LC, greater curvature and lesser curvature, respectively, of the ascending aortic arch; HRP, horseradish peroxidase; IAO, intercostal artery ostia; ICAM-2, intercellular adhesion molecule–2; LDL, low density lipoprotein; LOX-1, lectin-like oxidized LDL receptor–1; MCP-1, monocyte chemotactic protein–1; PI, propidium iodide; RAM, rabbit antimacrophage; VCAM-1, vascular cell adhesion molecule–1.

J. Jongstra-Bilen and M. Haidari contributed equally to this work.

M. Haidari's present address is Atherosclerosis Research Lab, Texas Heart Institute, Houston, TX 77030.


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