PACAP/PAC1R激活通过ERK通路促进2组先天性淋巴细胞依赖性过敏性鼻炎
Huigang Wang1, Yifei Ma1, Jianyao Li1
1Department of Otorhinolaryngology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, 561113, China.
Archives of biochemistry and biophysics
|July 25, 2025
概括
pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) 通过PAC1R-ERK通路激活2组先天性淋巴细胞 (ILC2s),从而促进过敏性鼻炎,从而加剧炎症.
科学领域:
- 免疫学 免疫学 免疫学
- 过敏研究 研究过敏
- 细胞生物学 细胞生物学
背景情况:
- 过敏性鼻炎 (AR) 是一种Th2介导的炎症性疾病.
- 第二组先天性淋巴细胞 (ILC2s) 参与AR的发病.
- 垂体腺酸环酶激活多 (PACAP) 在过敏炎症期间调节ILC2s中的作用尚不清楚.
研究的目的:
- 在过敏性炎症的背景下,研究PACAP对ILC2增殖的调节作用.
- 为了阐明参与PACAP介导ILC2激活的信号通路.
主要方法:
- 卵胺 (OVA) 诱导的AR小鼠模型用于体内研究.
- 使用ILC2细胞培养物的体外实验.
- PACAP和PAC1R的操纵 (敲击,对手),ERK通路分析 (p-ERK,PD98059) 的研究.
主要成果:
- 在OVA诱导的AR模型中,PACAP水平和ILC2种群的升高.
- PACAP促进了ILC2的增殖和IL-5和IL-13分泌子集的扩张.
- PACAP/PAC1R信号激活了ERK通路,导致ILC2扩散和细胞因子产生增加,加剧了AR.
- 抑制PACAP,PAC1R或ERK通路可以改善AR的病理特征.
结论:
- PACAP通过PAC1R-ERK信号通路促进ILC2的增殖和激活,从而加剧过敏性鼻炎.
- 针对PACAP/PAC1R/ERK轴提供了对过敏性鼻炎的潜在治疗策略.
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