Kidney int:IL-36R在肾脏缺血再灌注损伤的重要作用!

2017-12-17 MedSci MedSci原创

IL-36是IL-1细胞因子家族的新成员,包括3种亚型,IL-36α、IL-36β和IL-36γ,它们都含有IL-36受体的异二聚体。目前,关于IL-36轴在急性肾损伤(AKI)发病机制中的作用知之甚少。近期,一项发表在杂志Kidney int上的研究使用例IL-36R敲除小鼠和野生型小鼠建立双侧肾缺血再灌注AKI损伤模型,并评估了IL-36的功能。此项研究结果发现:IL-36R在肾中表达,主要在

IL-36是IL-1细胞因子家族的新成员,包括3种亚型,IL-36α、IL-36β和IL-36γ,它们都含有IL-36受体的异二聚体。目前,关于IL-36轴在急性肾损伤(AKI)发病机制中的作用知之甚少。

近期,一项发表在杂志Kidney int上的研究使用例IL-36R敲除小鼠和野生型小鼠建立双侧肾缺血再灌注AKI损伤模型,并评估了IL-36的功能。

此项研究结果发现:IL-36R在肾中表达,主要在近端小管中表达。在IL-36R敲除小鼠中,缺血再灌注损伤后血浆肌酐、血尿素氮和IL-6的水平显着低于野生型小鼠。免疫组织学分析显示了轻度肾小管损伤。缺血再灌注损伤后,IL-36α/β/γ的水平均升高,IL-36α在淋巴细胞和近端肾小管细胞中表达,而缺血再灌注损伤后IL-6和TNF-α的mRNA表达水平低于IL-36R敲除小鼠。

在肾小管上皮细胞的原代培养物中,IL-36α处理后可以上调NF-κB的活性和Erk磷酸化。值得注意的是,在AKI患者中,尿IL-36α的水平升高,并且肾活组织检查样品中的IL-36α染色也增强。

此项研究表明了IL-36α/IL-36R阻断可以作为AKI中潜在的治疗靶标。

原始出处:
Nishikawa H, Taniguchi Y, et al. Knockout of the interleukin-36 receptor protects against renal ischemia-reperfusion injury by reduction of proinflammatory cytokines. Kidney Int. 2017 Dec 11. pii: S0085-2538(17)30767-6. doi: 10.1016/j.kint.2017.09.017.

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