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(Circulation. 2001;103:2283.)
© 2001 American Heart Association, Inc.
Basic Science Reports |
High-Density Lipoprotein Loses Its Anti-Inflammatory Properties During Acute Influenza A Infection
From the Departments of Medicine (B.J.V.L., A.C.W., S.H., M.N., A.M.F.) and Microbiology, Immunology, and Molecular Genetics (D.P.N.), UCLA School of Medicine, Los Angeles, Calif.
Correspondence to Brian J. Van Lenten, PhD, Division of Cardiology, Department of Medicine, UCLA School of Medicine, 10833 Le Conte Avenue, Los Angeles, CA 90095-1679. E-mail bvanlent{at}mednet.ucla.edu
Background—Viruses have been identified as one of a variety of potential agents that are implicated in atherogenesis.
Methods and Results—C57BL/6J mice were killed before or 2, 3, 5, 7, or 9 days after intranasal infection with 105 plaque-forming units (pfu) of Influenza A strain WSN/33. Peak infectivity in lungs was reached by 72 hours, and it returned to baseline by 9 days. No viremia was observed at any time. The activities of paraoxonase and platelet-activating factor acetylhydrolase in HDL decreased after infection and reached their lowest levels 7 days after inoculation. The ability of HDL from infected mice to inhibit LDL oxidation and LDL-induced monocyte chemotactic activity in human artery wall cell cocultures decreased with time after inoculation. Moreover, as the infection progressed, LDL more readily induced monocyte chemotaxis. Peak interleukin-6 and serum amyloid A plasma levels were observed at 2 and 7 days after inoculation. HDL apoA-I levels did not change. ApoJ and ceruloplasmin levels in HDL peaked 3 days after infection. Ceruloplasmin remained elevated throughout the time course, whereas apoJ levels decreased toward baseline after the third day.
Conclusions—We conclude that alterations in the relative levels of paraoxonase, platelet-activating factor acetylhydrolase, ceruloplasmin, and apoJ in HDL occur during acute influenza infection, causing HDL to lose its anti-inflammatory properties.
Key Words: arteriosclerosis • infection • lipoproteins • mice • myocardial infarction
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