在Kiss1受体淘汰会加剧气道过敏反应和重塑在过敏喘的小鼠模型
Nilesh Sudhakar Ambhore1, Premanand Balraj1, Ashish Kumar1
1Department of Pharmaceutical Sciences, School of Pharmacy, College of Health and Human Sciences, North Dakota State University, Fargo, ND, 58102, USA.
Respiratory research
|October 29, 2024
概括
基斯丁受体 (Kiss1R) 信号传递对于调节喘至关重要. 失去Kiss1R会使呼吸道炎症,重塑和高反应性恶化,特别是在雌性小鼠中.
科学领域:
- 免疫学 免疫学 免疫学
- 肺部病理学 肺部病理学
- 内分泌学 在内分泌学.
背景情况:
- 性-类固醇信号关键调节喘病理生理学,但上游机制仍然不清楚.
- 以前的研究表明,kisspeptin (Kp) 和Kiss1R与呼吸道光滑肌肉重塑和高反应性有关.
- 这项研究研究了使用Kiss1R淘汰赛 (Kiss1R-/-) 小鼠在喘中内源性Kp的作用.
研究的目的:
- 在喘小鼠模型中,评估内源性kisspeptin信号对气道过敏反应 (AHR) 和气道重塑的影响.
- 确定Kiss1R缺乏对喘病理生理学的影响,特别是与性别差异有关.
主要方法:
- C57BL/6J野生型 (WT) 和Kiss1R-/-小鼠 (雄性和雌性) 受到混合过敏原 (MA) 的挑战.
- 通过使用 flexiVent 评估了呼吸道功能; 支气管 - 支气管洗 (BAL) 分析了免疫细胞和细胞因子.
- 组织学 (H&E,马森三染色体) 和免疫光学 (Ki-67,α-SMA,tenascin-c) 评估了气道重塑和炎症.
主要成果:
- 在MA挑战的小鼠中,Kiss1R的丧失加剧了肺功能和气道收缩性,女性的严重程度更高.
- Kiss1R-/-小鼠表现出免疫细胞透的增加,促炎细胞因子和Th2/Th17偏差细胞因子.
- 组织学发现Kiss1R-/-小鼠的原沉积和粘素产生增加,表明气道重塑和AHR加重.
结论:
- 内在的Kiss1R信号传递在控制气道炎症,AHR和喘重塑中发挥着至关重要的作用.
- 基斯佩丁受体信号传递是喘病理生理学的关键调节者.
- 向Kiss1R可能为喘管理提供治疗潜力.
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