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Published on: September 28, 2015
Inflammation and cellular immune responses in abdominal aortic aneurysms
Koichi Shimizu1, Richard N Mitchell, Peter Libby
1The Donald W. Reynolds Cardiovascular Clinical Research Center, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ksmz@rics.bwh.harvard.edu
Arteriosclerosis, Thrombosis, and Vascular Biology
|February 25, 2006
Summary
Abdominal aortic aneurysms (AAA) involve inflammation. Interferon-gamma (IFN-gamma) signaling deficiency promotes AAA, indicating a crucial role for Th1/Th2 balance in vascular disease.
Area of Science:
- Vascular Biology
- Immunology
- Atherosclerosis Pathophysiology
Background:
- Abdominal aortic aneurysms (AAA) and atherosclerotic lesions share inflammatory cell accumulation but differ in medial damage.
- Leukocyte recruitment and Th1 cytokines are typical in early atherogenesis, yet mechanistic differences between stenotic and aneurysmal disease remain unclear.
Purpose of the Study:
- To investigate the role of interferon-gamma (IFN-gamma) signaling in the development of abdominal aortic aneurysms (AAA).
- To explore the influence of Th1/Th2 cytokine balance on matrix remodeling in AAA pathophysiology.
Main Methods:
- Analysis of aortic allografts with deficient IFN-gamma signaling.
- Assessment of cytokine environments and matrix remodeling.
Main Results:
- Aortic allografts lacking IFN-gamma signaling developed AAA.
- AAA development correlated with a shift towards Th2 cytokine profiles.
Conclusions:
- IFN-gamma signaling plays a critical role in preventing AAA formation.
- Th1/Th2 cytokine balance is a key regulator of matrix remodeling and influences the distinct pathophysiologic mechanisms of aneurysmal versus occlusive vascular disease.
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