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J Pathol：CCL20阻断增加了肾毒性叶酸诱导的急性肾损伤的严重程度

2019-09-16 不详 网络

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趋化因子CCL20激活CCR6受体，并参与肾小球损伤的发病机制。然而，尚不清楚它会促进急性肾损伤（AKI）。我们鉴定CCL20在实验性毒性叶酸诱导的AKI的肾组织和应激培养的肾小管细胞的转录组学中表达上调，并探究了CCL20在实验和临床AKI中的表达和功能。在叶酸过量，顺铂或单侧输尿管梗阻诱导的三种肾损伤模型中证实CCL20的表达上调。在受损的肾脏中，CCL20在肾小管，内皮细胞和间质细胞中表达，

趋化因子CCL20激活CCR6受体，并参与肾小球损伤的发病机制。然而，尚不清楚它会促进急性肾损伤（AKI）。

我们鉴定CCL20在实验性毒性叶酸诱导的AKI的肾组织和应激培养的肾小管细胞的转录组学中表达上调，并探究了CCL20在实验和临床AKI中的表达和功能。

在叶酸过量，顺铂或单侧输尿管梗阻诱导的三种肾损伤模型中证实CCL20的表达上调。在受损的肾脏中，CCL20在肾小管，内皮细胞和间质细胞中表达，并且在人肾中也因AKI而表达上调。AKI患者的尿液中CCL20的水平增加，且水平与AKI严重性相关。通过使用中和抗CCL20抗体或CCR6缺陷小鼠评估CCL20在肾毒性叶酸诱导的AKI中的功能。结果显示，CCL20/CCR6靶向增加了肾衰竭的严重程度和患者死亡的风险。这与更严重的组织学损伤，肾钙质沉着，毛细血管稀疏和纤维化以及肾小管损伤相关基因的表达升高相关。令人惊讶的是，CCL20阻断的小鼠具有较低的管状增殖反应和较高数量的G2/M期细胞，表明修复机制受损。尽管在趋化因子表达和IL-17 +细胞和嗜中性粒细胞浸润方面有较轻微的炎症反应，但这可能与较低的Tregs流入有关。

总之，该研究结果表明CCL20在AKI期间通过减少组织损伤和促进修复来发挥肾脏保护作用。

原始出处：

González-Guerrero C, Morgado-Pascual JL, al., CCL20 blockade increases the severity of nephrotoxic folic acid-induced acute kidney injury. J Pathol. 2018 Oct;246(2):191-204. doi: 10.1002/path.5132. Epub 2018 Aug 27.

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    2020-02-14 41514497@qq.com

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    2019-09-18 yb6560

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    2019-09-18 zhouqu_8

    #肾毒性#

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