巨细胞介导IL4I1/AhR轴的激活是过敏性鼻炎的一个关键因素
Qian Liu1, Guohao Deng2, Xian Jiang2
1Department of Otolaryngology - Head and Neck Surgery, Third Xiangya Hospital, Central South University, Changsha 410013, Hunan, China; Department of Otolaryngology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215123, China.
International immunopharmacology
|March 13, 2025
概括
环境污染物可以引发过敏性鼻炎 (AR). IL4I1/Aryl碳化合物受体 (AhR) 轴促进M2巨细胞两极分化和上皮-介质细胞过渡 (EMT),恶化AR炎症.
科学领域:
- 免疫学 免疫学 免疫学
- 环境健康 环境健康
背景情况:
- 流行病学研究将环境污染物与过敏性鼻炎 (AR) 联系起来.
- 亚利碳化合物受体 (AhR) 参与免疫调节和M2巨细胞两极分化.
- 在AR病变发生过程中,AhR和M2巨细胞的机制尚未完全理解.
研究的目的:
- 研究IL4I1/AhR轴在过敏性鼻炎中的作用.
- 阐明该轴影响M2巨分化和上皮-介质细胞转换 (EMT) 的机制.
- 探索针对IL4I1/AhR通路的AR潜在的治疗策略.
主要方法:
- 公共数据集的生物信息分析 (GSE180697).
- 在患者样本 (鼻腔粘膜,单细胞,血清) 中进行验证,采用西部涂抹,qRT-PCR,免疫光和ELISA.
- 在人体初级细胞和THP-1细胞系的体外研究,包括M2巨诱导和IL4I1/AhR调节.
- 共同培养上皮细胞和巨细胞来评估EMT.
- 用AhR抑制剂或IL4I1调节器治疗的AR (卵泡诱导) 的小鼠模型.
主要成果:
- 在AR患者的单核细胞和鼻组织中激活了IL4I1/AhR轴.
- 激活AhR促进了IL4I1的上调,推动了M2巨细胞的两极分化.
- IL4I1/AhR轴调节了M2巨介导的EMT和IL-33/STAT6在上皮细胞中的信号传递.
- 在AR小鼠中,这个轴加剧了过敏症状和鼻子粘膜和肺部炎症.
结论:
- IL4I1/AhR轴是AR病变发生的关键参与者.
- 这个轴的激活促进M2巨细胞极化和EMT,导致炎症恶化.
- 针对IL4I1/AhR轴为AR提供了一个潜在的新疗法策略.
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