Interleukin-17 deficiency reduced vascular inflammation and development of atherosclerosis in Western diet-induced apoE-deficient mice |
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Authors: | Usui Fumitake Kimura Hiroaki Ohshiro Taichi Tatsumi Kazuki Kawashima Akira Nishiyama Akiyo Iwakura Yo-Ichiro Ishibashi Shun Takahashi Masafumi |
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Affiliation: | Division of Bioimaging Sciences, Center for Molecular Medicine, Japan. |
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Abstract: | ObjectiveSeveral reports describe the role of interleukin (IL)-17 in the development of atherosclerosis; however, its precise role remains controversial. We generated double-deficient mice for apolipoprotein E (apoE) and IL-17 (apoE?/?IL-17?/? mice) and investigated the effect of IL-17 deficiency on vascular inflammation and atherosclerosis.Methods and resultsAtherosclerotic plaque areas in apoE?/?IL-17?/? mice fed a Western diet (WD) were significantly reduced compared with those in apoE?/? mice. No significant differences in plasma lipid profiles were observed between apoE?/? and apoE?/?IL-17?/? mice. The number of infiltrated macrophages in the plaques was significantly decreased in WD-fed apoE?/?IL-17?/? mice compared with WD-fed apoE?/? mice, whereas vascular smooth muscle cell content was not altered by IL-17 deficiency. Expression of inflammatory cytokines (MCP-1, IL-1β, IL-6, IFN-γ, and IL-12 p40) and scavenger receptors (Msr-1, Scarb1, and Olr1) in the plaques was inhibited in WD-fed apoE?/?IL-17?/? mice. Furthermore, expression of inducible nitric oxide (M1 marker) and arginase-1 (M2 marker) was inhibited in WD-fed apoE?/?IL-17?/? mice.ConclusionOur results indicate that IL-17 deficiency reduces vascular inflammation and atherosclerosis and that modulation of IL-17 could be a potential target for prevention and treatment of atherosclerosis. |
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