on February 23, 2006
Published online before print February 23, 2006, doi: 10.1161/01.ATV.0000214999.12921.4f
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Submitted on September 1, 2005
Accepted on February 10, 2006
Inflammation and Cellular Immune Responses in Abdominal Aortic Aneurysms
Koichi Shimizu *;
From The Donald W. Reynolds Cardiovascular Clinical Research Center (K.S., P.L.), Cardiovascular Division, Department of Medicine and Department of Pathology (R.N.M.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.
* To whom correspondence should be addressed. E-mail: ksmz{at}rics.bwh.harvard.edu.
Abstract--Expansion and rupture of abdominal aortic aneurysms (AAA) result in high morbidity and mortality rates. Like stenotic atherosclerotic lesions, AAA accumulate inflammatory cells, but usually exhibit much more extensive medial damage. Leukocyte recruitment and expression of pro-inflammatory Th1 cytokines typically characterize early atherogenesis of any kind, and modulation of inflammatory mediators mutes atheroma formation in mice.
1 However, the mechanistic differences between stenotic and aneurysmal manifestations of atherosclerosis remain unexplained. We recently showed that aortic allografts deficient in interferon-
(IFN-) signaling developed AAA correlating with skewed Th2 cytokine environments, suggesting important regulatory roles for Th1/Th2 cytokine balance in modulating matrix remodeling and important implications for the pathophysiology of aortic aneurysm and atherosclerosis. Further probing of their distinct aspects of immune and inflammatory responses in vascular diseases should continue to shed new light on the pathophysiologic mechanisms that give rise to aneurysmal versus occlusive manifestations and atherosclerosis.
Key words: aortic aneurysm • cytokine • macrophages • pathogenesis • T-lymphocytes • transplantation
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