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趋化因子受体 5 阻断调节肾缺血再灌注损伤中的巨噬细胞迁移。

Chemokine receptor 5 blockade modulates macrophage trafficking in renal ischaemic-reperfusion injury.

机构信息

Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea.

Department of Internal Medicine, National Medical Center, Seoul, Korea.

出版信息

J Cell Mol Med. 2020 May;24(10):5515-5527. doi: 10.1111/jcmm.15207. Epub 2020 Mar 30.

DOI:10.1111/jcmm.15207
PMID:32227583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7214177/
Abstract

Chemokine receptor 5 (CCR5) is a pivotal regulator of macrophage trafficking in the kidneys in response to an inflammatory cascade. We investigated the role of CCR5 in experimental ischaemic-reperfusion injury (IRI) pathogenesis. To establish IRI, we clamped the bilateral renal artery pedicle for 30 min and then reperfused the kidney. We performed adoptive transfer of lipopolysaccharide (LPS)-treated RAW 264.7 macrophages following macrophage depletion in mice. B6.CCR5 mice showed less severe IRI based on tubular epithelial cell apoptosis than did wild-type mice. CXCR3 expression in CD11b cells and inducible nitric oxide synthase levels were more attenuated in B6.CCR5 mice. B6.CCR5 mice showed increased arginase-1 and CD206 expression. Macrophage-depleted wild-type mice showed more injury than B6.CCR5 mice after M1 macrophage transfer. Adoptive transfer of LPS-treated RAW 264.7 macrophages reversed the protection against IRI in wild-type, but not B6.CCR5 mice. Upon knocking out CCR5 in macrophages, migration of bone marrow-derived macrophages from wild-type mice towards primary tubular epithelial cells with recombinant CCR5 increased. Phospho-CCR5 expression in renal tissues of patients with acute tubular necrosis was increased, showing a positive correlation with tubular inflammation. In conclusion, CCR5 deficiency favours M2 macrophage activation, and blocking CCR5 might aid in treating acute kidney injury.

摘要

趋化因子受体 5（CCR5）是肾脏中巨噬细胞迁移的关键调节因子，可响应炎症级联反应。我们研究了 CCR5 在实验性缺血再灌注损伤（IRI）发病机制中的作用。为了建立 IRI，我们夹闭双侧肾动脉蒂 30 分钟，然后再灌注肾脏。我们在小鼠中进行了巨噬细胞耗竭后脂多糖（LPS）处理的 RAW 264.7 巨噬细胞的过继转移。与野生型小鼠相比，B6.CCR5 小鼠的肾小管上皮细胞凋亡的 IRI 程度较轻。B6.CCR5 小鼠的 CD11b 细胞中的 CXCR3 表达和诱导型一氧化氮合酶水平的降低更为明显。B6.CCR5 小鼠的精氨酸酶-1 和 CD206 表达增加。巨噬细胞耗竭的野生型小鼠在 M1 巨噬细胞转移后比 B6.CCR5 小鼠表现出更严重的损伤。过继转移 LPS 处理的 RAW 264.7 巨噬细胞逆转了对野生型但不是 B6.CCR5 小鼠的 IRI 保护作用。在巨噬细胞中敲除 CCR5 后，来自野生型小鼠的骨髓来源的巨噬细胞向重组 CCR5 的原代肾小管上皮细胞的迁移增加。急性肾小管坏死患者肾组织中磷酸化 CCR5 的表达增加，与肾小管炎症呈正相关。总之，CCR5 缺乏有利于 M2 巨噬细胞的激活，阻断 CCR5 可能有助于治疗急性肾损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/8009c31f94dc/JCMM-24-5515-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/39b999a5664a/JCMM-24-5515-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/0eead80528c0/JCMM-24-5515-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/ca65924a4338/JCMM-24-5515-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/5bb5aa7714fa/JCMM-24-5515-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/8009c31f94dc/JCMM-24-5515-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/39b999a5664a/JCMM-24-5515-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/33a4028250f7/JCMM-24-5515-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/ddac596ba6bc/JCMM-24-5515-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/97e5d68f9723/JCMM-24-5515-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/0eead80528c0/JCMM-24-5515-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/ca65924a4338/JCMM-24-5515-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c15/7214177/8009c31f94dc/JCMM-24-5515-g009.jpg

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