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(Circulation. 2006;113:920-922.)
© 2006 American Heart Association, Inc.

Editorial

Bacteria and Coronary Atheroma

More Fingerprints but No Smoking Gun

Joel T. Katz, MD; Richard P. Shannon, MD

From the Division of Infectious Diseases (J.T.K.), Brigham and Women’s Hospital, Boston, Mass, and the Department of Medicine (R.P.S.), Allegheny General Hospital, Pittsburgh, Pa.

Correspondence to Richard P. Shannon, MD, Department of Medicine, Allegheny General Hospital, 320 East North Ave, Pittsburgh, PA 15212. E-mail rshannon@wpahs.org

Key Words: Editorials • arteriosclerosis • infection • bacteria

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
For the better part of 2 decades, scientists from many disciplines have explored the role of innate and acquired immunity in mediating vascular atherosclerosis.^1–4 Remarkably, many of the distal mechanisms involved in the chronic inflammatory process that is atherosclerosis are mediated by the same cellular mechanisms that are "primed" to protect the body from microbial invasion. This recognizance against bacterial pathogens is embodied in the innate immune system that encodes more than 100 germ line–derived pattern recognition receptors (PRRs) designed to recognized highly conserved pathogen-associated molecular patterns. These receptors trigger effector mechanisms designed to phagocytize the foreign antigens and to call in reinforcements (memory B and T cells) provided by the adaptive immune system. Critical to the understanding of the role of the innate immune system in the pathogenesis of vascular atherosclerosis is the growing evidence that PRRs recognize "neoantigens" through the process of molecular mimicry. There are at least 4 candidate neoantigens that have been implicated in the atherosclerotic process.⁵ These include heat shock proteins, ß₂-glycoprotein-I, and, most notably, oxidized low-density lipoprotein (LDL) and related phospholipids. Oxidized LDL and phospholipids stimulate both natural immunoglobulin M antibodies, such as EO6, or other secreted PRRs, such as C-reactive protein, that have been identified as markers and mediators of chronic inflammation in atherosclerosis.⁶ Equally important has been the understanding of the role of a specialized group of PRRs known as scavenger receptors (CD36), which are present on monocytes, macrophages, and neutrophils that mediate the uptake of oxidized LDL and the generation . . . [Full Text of this Article]

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