Neutrophil-derived interleukin-17A participates in neuroinflammation induced by traumatic brain injury

作     者：Xiao-Jian Xu Qian-Qian Ge Meng-Shi Yang Yuan Zhuang Bin Zhang Jin-Qian Dong Fei Niu Hao Li Bai-Yun Liu Xiao-Jian Xu;Qian-Qian Ge;Meng-Shi Yang;Yuan Zhuang;Bin Zhang;Jin-Qian Dong;Fei Niu;Hao Li;Bai-Yun Liu

作者机构：Beijing Key Laboratory of Central Nervous System InjuryBeijing Neurosurgical InstituteCapital Medical UniversityBeijingChina Beijing Key Laboratory of Central Nervous System Injury and Department of NeurosurgeryBeijing Neurosurgical Institute and Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Nerve Injury and Repair Center of Beijing Institute for Brain DisordersBeijingChina China National Clinical Research Center for Neurological DiseasesBeijingChina 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2023年第18卷第5期

页      面：1046-1051页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 10[医学] 

基　　金：supported by the National Natural Science Foundation of China,No. 81771327 (to BYL) Construction of Central Nervous System Injury Basic Science and Clinical Translational Research Platform Budget of Beijing Municipal Health Commission 2020, No. PXM2020_026280_000002 (BYL)。 

主　　题：immune infiltration innate immunity interleukin-17A neurodegenerative disease neuroinflammation neutrophils secondary brain injury transcription factor transcriptome traumatic brain injury 

摘      要：After brain injury, infiltration and abnormal activation of neutrophils damages brain tissue and worsens inflammation, but the mediators that connect activated neutrophils with neuroinflammation have not yet been fully clarified. To identify regulators of neutrophil-mediated neuroinflammation after traumatic brain injury, a mouse model of traumatic brain injury was established by controlled cortical impact. At 7 days post-injury(sub-acute phase), genome-wide transcriptomic data showed that interleukin 17 A-associated signaling pathways were markedly upregulated, suggesting that interleukin 17 A may be involved in neuroinflammation. Double immunofluorescence staining showed that interleukin 17 A was largely secreted by neutrophils rather than by glial cells and neurons. Furthermore, nuclear factor-kappaB and Stat3, both of which are important effectors in interleukin 17 A-mediated proinflammatory responses, were significantly activated. Collectively, our findings suggest that neutrophil-derived interleukin 17 A participates in neutrophil-mediated neuroinflammation during the subacute phase of traumatic brain injury. Therefore, interleukin 17 A may be a promising therapeutic target for traumatic brain injury.