无感受神经元控制污染介导的中性恋喘
Jo-Chiao Wang1, Theo Crosson1, Amin Reza Nikpoor2,3
1Department of Pharmacology and Physiology, University de Montreal, Canada.
bioRxiv : the preprint server for biology
|September 4, 2024
概括
空气污染通过激活感官神经元,使喘恶化. 沉默这些神经元减少了呼吸道炎症,揭示了喘治疗的新治疗点.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 环境健康 环境健康
背景情况:
- 免疫系统和神经系统共享分子通路,影响恒常性.
- 神经元可以在喘等过敏性疾病中加剧炎症.
- 空气污染是已知的喘恶化因素之一.
研究的目的:
- 为了研究感觉神经元在污染加重的喘中的作用.
- 确定连接空气污染,神经元激活和呼吸道炎症的机制.
- 探索针对喘中神经元通路的治疗策略.
主要方法:
- 鼠被暴露在环境PM2.5颗粒和卵胺中,以模拟污染加重的喘.
- 在支气管支气管洗液中测量了中性粒细胞和玛三角形T细胞水平.
- 使用鼻内QX-314或TRPV1神经元切除,可以使知觉神经元保持沉默.
- 评估了TRPA1通道灵敏度,阿尔特明水平和巨细胞激活.
主要成果:
- 在喘小鼠中,PM2.5暴露显著增加了中性粒细胞和γδ T 细胞.
- 沉默感应神经元或消灭TRPV1神经元使呼吸道炎症和中性粒细胞数量正常化.
- 暴露于污染的小鼠表现出TRPA1通道敏感度升高和高胺水平.
- 表达状碳化合物受体的膜巨细胞被确定为artemin的来源.
结论:
- 空气污染激活了肺内置性感受神经元,从而加剧了喘.
- 巨细胞释放的阿尔特明增强了神经元的TRPA1反应能力,增加了中性粒细胞的流入.
- 准 nociceptor神经元为喘中污染诱导的中性恋呼吸道炎症提供了一个潜在的治疗策略.
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