在慢性喘模型中,IL-36通过诱导表皮层-介质细胞过渡过程,参与了呼吸道重塑
Min Zhang1,2, Jiemei Cen1, Wenlei Gan1
1Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Disease of Sun Yat-Sen University, Third Affiliated Hospital of Sun Yat-Sen University, Tianhe Road 600, Guangzhou, 510630, Guangdong, China.
干白素-36 (IL-36) 通过诱导上皮层-介质细胞过渡 (EMT) 来促进严重喘中的呼吸道重塑. 阻断IL-36信号减轻了与喘相关的气道改造和炎症,这表明IL-36是潜在的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 肺部病理学 肺部病理学
- 细胞生物学 细胞生物学
背景情况:
- 严重的喘的特征是呼吸道重塑,这是一种涉及表皮-介质细胞过渡 (EMT) 的过程.
- 干白素-36 (IL-36),一种IL-1家族成员,与过敏性疾病有关,但其在喘相关的气道改造中的作用尚未完全理解.
研究的目的:
- 为了研究IL-36对EMT在气道上皮细胞中的作用.
- 为了确定是否抑制IL-36诱导的EMT可以减轻严重喘中的呼吸道重塑.
主要方法:
- 用IL-36受体 (IL-36R) 激素刺激BEAS-2B细胞,以评估EMT标记物和细胞迁移.
- 用一种慢性喘小鼠模型来评估IL-36信号对气道炎症和重塑的影响.
主要成果:
- 在BEAS-2B细胞中,IL-36诱导了EMT和增强了细胞迁移,同时促进了NF-κB和STAT3酸化.
- 在体内,IL-36受体对抗剂 (IL-36Ra) 治疗减少了炎症细胞的透,降低了气道过敏反应 (AHR),并通过抑制喘小鼠的EMT缓解了气道重塑.
- 同时使用IL-36R激活剂与IL-36Ra,可逆转与气道重塑相关的病理变化.
结论:
- 通过诱导EMT,IL-36信号传递有助于重症喘时的气道改造.
- IL-36代表了一种新的治疗点,用于在严重喘中管理呼吸道重塑.
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