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Interleukin-17 deficiency reduced vascular inflammation and development of atherosclerosis in Western diet-induced apoE-deficient mice
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摘要

Objective

Several 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鈭?鈭?/sup>IL-17鈭?鈭?/sup> mice) and investigated the effect of IL-17 deficiency on vascular inflammation and atherosclerosis.

Methods and results

Atherosclerotic plaque areas in apoE鈭?鈭?/sup>IL-17鈭?鈭?/sup> mice fed a Western diet (WD) were significantly reduced compared with those in apoE鈭?鈭?/sup> mice. No significant differences in plasma lipid profiles were observed between apoE鈭?鈭?/sup> and apoE鈭?鈭?/sup>IL-17鈭?鈭?/sup> mice. The number of infiltrated macrophages in the plaques was significantly decreased in WD-fed apoE鈭?鈭?/sup>IL-17鈭?鈭?/sup> mice compared with WD-fed apoE鈭?鈭?/sup> mice, whereas vascular smooth muscle cell content was not altered by IL-17 deficiency. Expression of inflammatory cytokines (MCP-1, IL-1尾, IL-6, IFN-纬, and IL-12 p40) and scavenger receptors (Msr-1, Scarb1, and Olr1) in the plaques was inhibited in WD-fed apoE鈭?鈭?/sup>IL-17鈭?鈭?/sup> mice. Furthermore, expression of inducible nitric oxide (M1 marker) and arginase-1 (M2 marker) was inhibited in WD-fed apoE鈭?鈭?/sup>IL-17鈭?鈭?/sup> mice.

Conclusion

Our 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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