Lack of Interleukin-1&bgr; Decreases the Severity of Atherosclerosis in ApoE-Deficient Mice

By H. Kirii, T. Niwa, Yasuhiro Yamada, H. Wada, Kuniaki Saito, Y. Iwakura, M. Asano, H. Moriwaki, M. Seishima. Arteriosclerosis, Thrombosis and Vascular Biology, 2003

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Objective—Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis. We focused on the role of interleukin-1&bgr; (IL-1&bgr;), one of the proinflammatory cytokines secreted by monocytes/macrophages, in the progression of atherosclerosis. Methods and Results—We generated mice lacking both apoE and IL-1&bgr;. The sizes of atherosclerotic lesions at the aortic sinus in apoE−/−/IL-1&bgr;−/−mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE−/−/IL-1&bgr;+/+ mice, and the percentage of the atherosclerotic area to total area of apoE−/−/IL-1&bgr;−/− at 24 weeks of age also showed a significant decrease of about 30% compared with apoE−/−/IL-1&bgr;+/+. The mRNA levels of vascular cell adhesion molecule (VCAM)-1 and monocyte chemotactic protein-1 in the apoE−/−/IL-1&bgr;−/− aorta were significantly reduced compared with the apoE−/−/IL-1&bgr;+/+. Furthermore, VCAM-1 was also reduced at the protein level in apoE−/−/IL-1&bgr;−/− aorta compared with apoE−/−/IL-1&bgr;+/+. Conclusions—The lack of IL-1&bgr; decreases the severity of atherosclerosis in apoE deficient mice, possibly through increased expressions of VCAM-1 and monocyte chemotactic protein-1 in the aorta.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/830c97c506e4344577d9d78596c31d80d2591b86

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