Published Online
on July 8, 2002

A more recent version of this article appeared on July 23, 2002

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Submitted on March 26, 2002
Revised on May 8, 2002
Accepted on May 9, 2002

Cross-Reactivity of Anti-CagA Antibodies With Vascular Wall Antigens. Possible Pathogenic Link Between Helicobacter pylori Infection and Atherosclerosis

Francesco Franceschi MD, Antonia R. Sepulveda MD, Antonio Gasbarrini MD, Paolo Pola MD, Nicolò Gentiloni Silveri MD, Giovanni Gasbarrini MD, David Y. Graham MD, and Robert M. Genta MD^*

From the Departments of Pathology (F.F., R.M.G.) and Medicine (D.Y.G., R.M.G.), VA Medical Center and Baylor College of Medicine, Houston, Tex; Department of Pathology (A.R.S.), University of Pittsburgh, Pittsburgh, Pa; and Department of Internal Medicine (F.F., A.G., P.P., N.G.S., G.G.), Catholic University of Rome, Italy.

^* To whom correspondence should be addressed. E-mail: rmgenta{at}bcm.tmc.edu.

Background—Helicobacter pylori-CagA positive strains have been shown to be associated with atherosclerosis. However, the pathogenesis is still undetermined. The aim of this study was to determine whether anti-CagA antibodies cross-react with antigens of normal and atherosclerotic arteries.

Methods and Results—Eight umbilical cord sections, 14 atherosclerotic artery sections, and 10 gastrointestinal tract sections were examined by immunohistochemistry using polyclonal anti-CagA antibodies. Five atherosclerotic and 3 normal artery samples were also lysed in ice-cold lysis buffer containing protease inhibitors and were immunoprecipitated using the same antibodies. Anti-CagA antibodies reacted with cytoplasm and nuclei of smooth muscle cells in umbilical cord and atherosclerotic vessel sections, cytoplasm of fibroblasts-like cells in intimal atherosclerotic plaques, and the cell membranes of endothelial cells. Anti-CagA antibodies also specifically immunoprecipitated 2 high molecular weight antigens of 160 and 180 kDa from both normal and atherosclerotic artery lysates.

Conclusions—Anti-CagA antibodies cross-react with antigens of both normal and atherosclerotic blood vessels. We speculate that the binding of anti-CagA antibodies to those antigens in injured arteries could influence the progression of atherosclerosis in CagA-positive H pylori-infected patients.

Key words: atherosclerosis • infection • antibodies

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