HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chan, W. C. Articles by Yeung, R. S. M. Search for Related Content PubMed PubMed Citation Articles by Chan, W. C. Articles by Yeung, R. S. M.

Presence of IFN- Does Not Indicate Its Necessity for Induction of Coronary Arteritis in an Animal Model of Kawasaki Disease¹

Wesley C. Chan^2,*, Trang T. Duong^2,* and Rae S. M. Yeung^3,*,

^* Division of Cancer Research, Hospital for Sick Children Research Institute, Toronto, Canada; and Division of Rheumatology, Department of Paediatrics, Hospital for Sick Children, University of Toronto, Toronto, Canada

Kawasaki disease is the most common cause of vasculitis affecting children, and the leading cause of acquired heart disease in the developed world. To date, studies on the role of IFN- in the pathogenesis of Kawasaki disease have focused on peripheral production of IFN-, and have yielded conflicting results. Affected heart tissue is not available from children with Kawasaki disease. In this study, we use an animal model of Kawasaki disease, Lactobacillus casei cell wall extract (LCWE)-induced coronary arteritis, to examine the role of IFN- in the development of coronary artery lesions. We report the presence of IFN-, both at the mRNA and protein levels, in the affected vessels. Its biphasic expression, first at days 3–7 and again at days 28–42 post-LCWE injection, corresponds to the first appearance of inflammatory infiltrate in coronary arteries, and later to vascular wall disruption and aneurysm formation, respectively. Interestingly, ablation of IFN- expression did not dampen the inflammatory response, and IFN--deficient lymphocytes proliferated more vigorously in response to LCWE than those of wild-type animals. Of more importance, the incidence of coronary arteritis was the same in IFN--deficient and wild-type mice. Taken together, our findings demonstrate that IFN- regulates the immune response during development of coronary arteritis, but is not required for the induction of coronary artery disease.

This article has been cited by other articles:

				J. S. Hui-Yuen, T. T. Duong, and R. S. M. Yeung TNF-{alpha} Is Necessary for Induction of Coronary Artery Inflammation and Aneurysm Formation in an Animal Model of Kawasaki Disease J. Immunol., May 15, 2006; 176(10): 6294 - 6301. [Abstract] [Full Text] [PDF]

				M. E. Rosenkranz, D. J. Schulte, L. M.A. Agle, M. H. Wong, W. Zhang, L. Ivashkiv, T. M. Doherty, M. C. Fishbein, T. J.A. Lehman, K. S. Michelsen, et al. TLR2 and MyD88 Contribute to Lactobacillus casei Extract-Induced Focal Coronary Arteritis in a Mouse Model of Kawasaki Disease Circulation, November 8, 2005; 112(19): 2966 - 2973. [Abstract] [Full Text] [PDF]