卡尔蛋白蛋白是由IL-17A调节的,并诱导喘中的类固醇低响应性
Narjes Saheb Sharif-Askari1,2, Bushra Mdkhana1, Shirin Hafezi1
1Research Institute for Medical and Health Sciences, College of Medicine, University of Sharjah, Sharjah, United Arab Emirates.
概括
在严重喘中,calprotectin (S100A8 / S100A9) 的高调,有助于降低类固醇反应. 在临床前模型中,用帕基尼莫德抑制calprotectin可降低炎症并恢复类固醇敏感性.
科学领域:
- 免疫学 免疫学 免疫学
- 肺部病理学 肺部病理学
- 药理学 药理学是指药理学的学科.
背景情况:
- 卡尔蛋白蛋白 (S100A8/S100A9) 与喘等炎症性疾病有关.
- 它的调节和在严重喘中对类固醇反应过低的作用尚不清楚.
研究的目的:
- 研究IL-17对calprotectin的调节.
- 确定calprotectin在类固醇低反应性中的作用.
- 评估帕基尼莫德作为治疗类固醇耐药喘的治疗剂.
主要方法:
- 在人类支气管纤维细胞和小鼠模型中评估了calprotectin表达.
- 用IL-17A刺激细胞和评估的类固醇反应标志物.
- 在室内灰尘虫/cdiGMP诱导的小鼠喘模型中使用帕基尼莫德.
主要成果:
- 喘性纤维细胞显示出比对照组更高的calprotectin;IL-17增加了calprotectin和失调的类固醇特征.
- 在小鼠中,Paquinimod逆转了IL-17的影响,减少了呼吸道炎症,并恢复了类固醇特征.
- 帕基尼莫德抑制了MAPK/ERK和NF-κB通路,与德克萨米他不同,其有效性有限.
结论:
- 通过IL-17调节的calprotectin是类固醇低反应性喘的关键参与者.
- 向calprotectin提供了一种潜在的策略,以改善严重喘中的炎症和类固醇敏感性.
- 需要进一步的研究来探索临床应用和类固醇机制相互作用.
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