The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/12/1733/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 12, December 20, 1999 1733-1740

Original Article

C-Reactive Protein and Complement Are Important Mediators of Tissue Damage in Acute Myocardial Infarction

M. Grisellia,b, J. Herberta, W.L. Hutchinsona, K.M. Taylorb, M. Sohailc, T. Krauszc, and M.B. Pepysa

a Immunological Medicine Unit, Division of Medicine,
b Cardiothoracic Unit, Department of Surgery
c Department of Histopathology, Imperial College School of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom
Dept. of Medicine, Royal Free Campus, Royal Free and University College Medical School, Rowland Hill St., London NW3 2PF, UK.44-20-7472-280344-20-7472-2801

m.pepys{at}rfc.ucl.ac.uk

Myocardial infarction in humans provokes an acute phase response, and C-reactive protein (CRP), the classical acute phase plasma protein, is deposited together with complement within the infarct. The peak plasma CRP value is strongly associated with postinfarct morbidity and mortality. Human CRP binds to damaged cells and activates complement, but rat CRP does not activate complement. Here we show that injection of human CRP into rats after ligation of the coronary artery reproducibly enhanced infarct size by ~40%. In vivo complement depletion, produced by cobra venom factor, completely abrogated this effect. Complement depletion also markedly reduced infarct size, even when initiated up to 2 h after coronary ligation. These observations demonstrate that human CRP and complement activation are major mediators of ischemic myocardial injury and identify them as therapeutic targets in coronary heart disease.

Key Words: heart • ischemia • necrosis • inflammation • acute phase response

Abbreviations used in this paper: CRP, C-reactive protein; NBT, nitroblue tetrazolium; SAP, serum amyloid P component.

© 1999 The Rockefeller University Press


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