on January 30, 2003
Arteriosclerosis, Thrombosis, and Vascular Biology. 2003
Published online before print January 30, 2003, doi: 10.1161/01.ATV.0000059419.11002.6E
Published online before print January 30, 2003, doi: 10.1161/01.ATV.0000059419.11002.6E
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Submitted on September 10, 2002
Accepted on December 18, 2002
Influence of Interferon-
on the Extent and Phenotype of Diet-Induced Atherosclerosis in the LDLR-Deficient Mouse
Chiara Buono ;
From the Immunology Research Division (C.B., C.E.C., A.H.L.) and the Vascular Research Division (G.S., A.H.L.), Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass; and the J. Alick Little Lipid Research Laboratory, St Michael's Hospital, and the Departments of Laboratory Medicine and Pathobiology, Biochemistry, and Medicine (G.F.M., P.W.C.), University of Toronto, Toronto, Canada.
* To whom correspondence should be addressed. E-mail: alichtman{at}rics.bwh.harvard.edu.
Objective--The aim of this study was to investigate the influence of interferon-
(IFN-) on atherosclerosis in low density lipoprotein receptor (LDLR)-null mice.
Methods and Results--We cross-bred IFN--deficient mice with LDLR-null mice and analyzed lipoprotein profiles and atherosclerosis in the compound mutant progeny after 8 and 20 weeks on a cholesterol-enriched diet. IFN- deficiency did not affect serum cholesterol levels or lipoprotein profiles, but it did affect the extent and phenotype of atherosclerosis. Atherosclerotic lesions in IFN--deficient mice were reduced by 75% in the aortic arch and by 46% in the descending aorta compared with control mice after 8 weeks on the diet. After 20 weeks, arch lesions were reduced by 43%, and descending aorta lesions were reduced by 65% in IFN--deficient mice compared with controls. At 8 weeks, percent lesional macrophage and smooth muscle content was significantly less in the IFN--deficient mice, but not at 20 weeks. Although there were fewer class II major histocompatibility complex-positive cells in the lesions of IFN--deficient animals compared with controls, class II major histocompatibility complex expression on endothelial cells overlying lesions persisted in the absence of IFN-.
Conclusions--These data provide direct evidence that IFN- influences atherosclerosis development and phenotype in the LDLR-deficient mouse, independent of changes in blood lipoprotein profiles.
Key words: atherosclerosis • cytokines • endothelium • mouse • T cells
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