三叉神经节中与老化相关的巨噬细胞极化会加剧切口口内疼痛

IF 2.9 3区 医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
Oral diseases Pub Date : 2025-02-01 Epub Date: 2024-10-28 DOI:10.1111/odi.15165
Kentaro Urata, Tatsuki Oto, Yoshinori Hayashi, Suzuro Hitomi, Takayuki Ikeda, Koichi Iwata, Toshimitsu Iinuma, Masamichi Shinoda
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引用次数: 0

摘要

目的:虽然三叉神经节(TG)中的巨噬细胞极化对口面部痛觉过敏至关重要,但与衰老相关的变化及其对口内痛觉过敏的影响仍不清楚。我们使用衰老加速小鼠(SAM)易感性8(SAMP8)和SAM抗性1(SAMR1)评估了TG中与衰老相关的巨噬细胞极化对腭粘膜切口后口内机械痛觉过敏的影响:腭粘膜切口后 21 天测量腭粘膜的机械性缩头反射阈值(MHWRT)。在第 3 天和第 14 天,分析了 TG 中 Iba-1 免疫反应(IR)细胞、CD11c-IR 细胞(促炎巨噬细胞(M1))、C-C 矩阵趋化因子配体 2(CCL2)-IR M1-巨噬细胞、CD206-IR 细胞(抗炎巨噬细胞(M2))和转化生长因子-β(TGF-β)-IR M2-巨噬细胞的丰度。研究还考察了在 TG 内持续给予 CCL2 中和抗体或重组-CCL2 对 MHWRT 的影响:结果:与SAMR1相比,切口诱导的MHWRT下降在SAMP8中有所增强。在第 3 天和第 14 天,与 SAMR1 相比,SAMP8 中 TG 中 CCL2-IR M1 巨噬细胞的数量增加。CCL2中和抗体抑制了SAMP8的痛觉过敏性,而重组CCL2则增加了痛觉过敏性:结论:口腔黏膜损伤后的机械痛觉过敏会通过 TG 中与年龄相关的 M1-巨噬细胞过度激活增强 CCL2 信号,从而增强和维持痛觉过敏。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ageing-Related Macrophage Polarisation in the Trigeminal Ganglion Enhances Incisional Intraoral Pain.

Objective: Although macrophage polarisation in the trigeminal ganglion (TG) is crucial in orofacial pain hypersensitivity, the effect of ageing-related changes and their involvement in intra-oral nociception remains unclear. We assessed the effect of ageing-related macrophage polarisation in TG on intra-oral mechanical pain hypersensitivity following palatal mucosal incision using senescence-accelerated mice (SAM)-prone8 (SAMP8) and SAM-resistant 1 (SAMR1).

Materials and methods: Mechanical head-withdrawal reflex threshold (MHWRT) of the palatal mucosa was measured for 21 days after palatal mucosal incision. On days 3 and 14, the abundance of Iba-1-immunoreactive (IR) cells, CD11c-IR cells (pro-inflammatory macrophages (M1)), C-C motif chemokine ligand 2 (CCL2)-IR M1-macrophages, CD206-IR cells (anti-inflammatory macrophages (M2)) and transforming growth factor-β (TGF-β)-IR M2-macrophages in the TG was analysed. The effect of continuous intra-TG administration of CCL2-neutralising antibody or recombinant-CCL2 on MHWRT was examined.

Results: Incision-induced decrease in MHWRT was enhanced in SAMP8 compared with that in SAMR1. On days 3 and 14, the number of CCL2-IR M1-macrophages in TG was increased in SAMP8 compared with that in SAMR1. CCL2-neutralising antibody suppressed, whereas recombinant-CCL2 increased pain hypersensitivity in SAMP8.

Conclusions: Mechanical pain hypersensitivity after oral mucosal injury is potentiated and sustained by age-related enhancement of CCL2 signalling via M1-macrophage hyperactivation in TG.

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来源期刊
Oral diseases
Oral diseases 医学-牙科与口腔外科
CiteScore
7.60
自引率
5.30%
发文量
325
审稿时长
4-8 weeks
期刊介绍: Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.
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