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三叉神经节初级感觉神经元中的趋化因子受体CXCR2介导口面部瘙痒。

Chemokine receptor CXCR2 in primary sensory neurons of trigeminal ganglion mediates orofacial itch.

作者信息

Li Dong-Jin, Zhong Zhen-Juan, Wang Xiao-Liang, Wei Na, Zhao Si-Jia, Shan Ting-Ting, Liu Ya-Ping, Yu Yao-Qing

机构信息

College of Life Sciences, Northwest University, Xi'an, China.

Institute for Biomedical Sciences of Pain, Tangdu Hospital, Air Force Medical University, Xi'an, China.

出版信息

Front Mol Neurosci. 2023 Oct 26;16:1279237. doi: 10.3389/fnmol.2023.1279237. eCollection 2023.

DOI:10.3389/fnmol.2023.1279237
PMID:37953876
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10637378/
Abstract

The CXCR2 chemokine receptor is known to have a significant impact on the initiation and control of inflammatory processes. However, its specific involvement in the sensation of itch is not yet fully understood. In this study, we aimed to elucidate the function of CXCR2 in the trigeminal ganglion (TG) by utilizing orofacial itch models induced by incision, chloroquine (CQ), and histamine. Our results revealed a significant up-regulation of CXCR2 mRNA and protein expressions in the primary sensory neurons of TG in response to itch stimuli. The CXCR2 inhibitor SB225002 resulted in notable decrease in CXCR2 protein expression and reduction in scratch behaviors. Distal infraorbital nerve (DION) microinjection of a specific shRNA virus inhibited CXCR2 expression in TG neurons and reversed itch behaviors. Additionally, the administration of the PI3K inhibitor LY294002 resulted in a decrease in the expressions of p-Akt, Akt, and CXCR2 in TG neurons, thereby mitigating pruritic behaviors. Collectively, we report that CXCR2 in the primary sensory neurons of trigeminal ganglion contributes to orofacial itch through the PI3K/Akt signaling pathway. These observations highlight the potential of molecules involved in the regulation of CXCR2 as viable therapeutic targets for the treatment of itch.

摘要

已知CXCR2趋化因子受体对炎症过程的启动和控制有重大影响。然而，其在瘙痒感觉中的具体作用尚未完全明确。在本研究中，我们旨在通过利用由切割、氯喹（CQ）和组胺诱导的口面部瘙痒模型，阐明CXCR2在三叉神经节（TG）中的功能。我们的结果显示，在瘙痒刺激下，TG初级感觉神经元中CXCR2 mRNA和蛋白表达显著上调。CXCR2抑制剂SB225002导致CXCR2蛋白表达显著降低，并减少抓挠行为。向眶下神经（DION）远端微量注射特异性shRNA病毒可抑制TG神经元中CXCR2的表达，并逆转瘙痒行为。此外，给予PI3K抑制剂LY294002会导致TG神经元中p-Akt、Akt和CXCR2的表达降低，从而减轻瘙痒行为。总体而言，我们报告三叉神经节初级感觉神经元中的CXCR2通过PI3K/Akt信号通路促成口面部瘙痒。这些观察结果突出了参与CXCR2调节的分子作为治疗瘙痒的可行治疗靶点的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/79f1cb0e16e5/fnmol-16-1279237-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/8a714d8ea9fa/fnmol-16-1279237-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/45cd071dd780/fnmol-16-1279237-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/ff84e1615371/fnmol-16-1279237-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/24d2128d5bec/fnmol-16-1279237-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/79f1cb0e16e5/fnmol-16-1279237-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/8a714d8ea9fa/fnmol-16-1279237-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/45cd071dd780/fnmol-16-1279237-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/ff84e1615371/fnmol-16-1279237-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/24d2128d5bec/fnmol-16-1279237-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d3/10637378/79f1cb0e16e5/fnmol-16-1279237-g005.jpg

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