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CXCR2 对于辐射诱导的肠道损伤是必需的，它通过引发中性粒细胞浸润来实现。

CXCR2 Is Essential for Radiation-Induced Intestinal Injury by Initiating Neutrophil Infiltration.

机构信息

Department of Radiation Oncology, The Second Affiliated Hospital of Soochow University, Suzhou 215000, China.

Department of Radiation Oncology, Affiliated Hospital of Jiangsu University, Zhenjiang 212000, China.

出版信息

J Immunol Res. 2022 Jul 16;2022:7966089. doi: 10.1155/2022/7966089. eCollection 2022.

DOI:10.1155/2022/7966089
PMID:35879949
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9308512/
Abstract

Neutrophils, known as an important part of the immune system, are the most abundant leukocyte population in peripheral blood, but excessive recruitment will lead to tissue/organ injury. RNA sequencing showed that ionizing radiation significantly increased the expression of characteristic genes of neutrophils in intestinal tissues compared with liver and lung tissues. By clearing neutrophils with an anti-Ly6G antibody, we found that neutrophil infiltration is critical for irradiation-induced intestinal injury. CXCR2 is a G-protein-coupled receptor that mediates the migration of neutrophils by combining with its ligands. Compared with observations in liver and lung tissues, we found that CXCR2 and its ligands, including CXCL1, CXCL2, CXCL3, and CXCL5, were all significantly upregulated in irradiated intestinal tissues. Further studies showed that SB225002, an inhibitor of CXCR2, could effectively inhibit the chemotaxis of neutrophils and tissue damage mediated by the CXCL-CXCR2 signalling pathway.

摘要

中性粒细胞作为免疫系统的重要组成部分，是外周血中最丰富的白细胞群体，但过度募集会导致组织/器官损伤。RNA 测序显示，与肝组织和肺组织相比，电离辐射显著增加了肠道组织中中性粒细胞特征基因的表达。通过使用抗 Ly6G 抗体清除中性粒细胞，我们发现中性粒细胞浸润对于辐射诱导的肠道损伤至关重要。CXCR2 是一种 G 蛋白偶联受体，通过与配体结合介导中性粒细胞的迁移。与肝组织和肺组织的观察结果相比，我们发现 CXCR2 及其配体，包括 CXCL1、CXCL2、CXCL3 和 CXCL5，在辐射后的肠道组织中均显著上调。进一步的研究表明，CXCR2 的抑制剂 SB225002 可有效抑制中性粒细胞的趋化作用以及由 CXCL-CXCR2 信号通路介导的组织损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/e0fdce64ab47/JIR2022-7966089.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/6402afcc544d/JIR2022-7966089.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/1b6a8c53fbfb/JIR2022-7966089.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/2e040981c889/JIR2022-7966089.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/e0fdce64ab47/JIR2022-7966089.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/6402afcc544d/JIR2022-7966089.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/1b6a8c53fbfb/JIR2022-7966089.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/2e040981c889/JIR2022-7966089.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/766e/9308512/e0fdce64ab47/JIR2022-7966089.004.jpg

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