Pharmacological Inhibition of CCR2 Signaling Exacerbates Exercise-Induced Inflammation Independently of Neutrophil Infiltration and Oxidative Stress
Pharmacological Inhibition of CCR2 Signaling Exacerbates Exercise-Induced Inflammation Independently of Neutrophil Infiltration and Oxidative Stress
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DOI：
10.3390/immuno2010003
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发表时间：
2022-03-01
期刊：
影响因子：
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通讯作者：
Suzuki, Katsuhiko
中科院分区：
文献类型：
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作者：
Tominaga, Takaki;Huang, Jiapeng;Suzuki, Katsuhiko
虽然运动诱导的体液因子被称为运动因子有益于全身健康，但大多数运动因子的作用尚未被研究。单核细胞趋化蛋白-1（MCP-1）是一种运动后循环浓度升高的典型趋化因子，是运动因子之一。MCP-1是CC趋化因子受体2（CCR 2）的配体，CCR 2在单核细胞、巨噬细胞和肌肉细胞上表达。然而，没有关于CCR 2信号在运动中的作用的信息。因此，为了探讨这一研究问题，我们在运动前后给小鼠注射CCR 2拮抗剂或PBS来抑制CCR 2信号。我们的研究结果表明，CCR 2信号抑制促进运动诱导的巨噬细胞浸润和炎症后24小时在肌肉中运动。CCR 2信号传导抑制也加剧了运动后立即在肌肉中运动诱导的炎症。然而，中性粒细胞浸润和氧化应激没有贡献运动诱导的炎症CCR 2信号抑制。CCR 2信号传导抑制也加剧了运动后立即在肾脏，肝脏和脂肪组织中运动诱导的炎症。总而言之，CCR 2信号传导的药理学抑制会加剧运动诱导的炎症，与中性粒细胞浸润和氧化应激无关。
Although exercise-induced humoral factors known as exerkines benefit systemic health, the role of most exerkines has not been investigated. Monocyte chemoattractant protein-1 (MCP-1) is a representative chemokine whose circulating concentrations increase after exercise, and it is one of the exerkines. MCP-1 is a ligand for CC chemokine receptor 2 (CCR2), which is expressed on monocytes, macrophages, and muscle cells. However, there is no information on the role of CCR2 signaling in exercise. Therefore, to investigate the research question, we administrated CCR2 antagonist or PBS to mice to inhibit CCR2 signaling before and after exercise. Our results showed that CCR2 signaling inhibition promoted exercise-induced macrophage infiltration and inflammation 24 h after exercise in muscle. CCR2 signaling inhibition also exacerbated exercise-induced inflammation immediately after exercise in muscle. However, neutrophil infiltration and oxidative stress had no contribution to exercise-induced inflammation by CCR2 signaling inhibition. CCR2 signaling inhibition also exacerbated exercise-induced inflammation immediately after exercise in kidney, liver, and adipose tissues. To summarize, pharmacological inhibition of CCR2 signaling exacerbated exercise-induced inflammation independently of neutrophil infiltration and oxidative stress.