支气管上皮质中的病毒复制和干扰素反应由Th17细胞增强
Weston T Powell1,2, Tomasz J Janczyk3, Patricia C Dela Cruz1,4
1Center for Respiratory Biology and Therapeutics, Seattle Children's Research Institute, Seattle, WA., USA.
在患有喘的儿童中,Th17淋巴细胞在淋巴病毒感染期间促进呼吸道上皮干扰素反应. 这项研究揭示了Th17细胞如何影响喘恶化和病毒免疫力.
科学领域:
- 免疫学 免疫学 免疫学
- 呼吸系统医学 呼吸系统医学
- 分子生物学分子生物学
背景情况:
- 喘是一种慢性呼吸道疾病,其特点是气道炎症.
- Th17淋巴细胞在喘病原发生过程中发挥作用.
- 在喘中,Th17细胞与表皮对鼻病毒的反应之间的相互作用尚未得到充分理解.
研究的目的:
- 为了研究Th17淋巴细胞对支气管上皮细胞对小儿喘中犀病毒 (RV) 感染的反应的影响.
- 在RV感染和Th17初始化后,对支气管上皮细胞 (BECs) 和Th17细胞的基因表达变化的特征.
主要方法:
- 来自喘儿童的器官类型支气管上皮细胞 (BEC) 培养与健康的 Th17 淋巴细胞共同培养.
- 培养物在人类犀牛病毒-16 (RV-16) 冠状病毒感染前4天进行了原始化.
- 用RNA测序和权重基因联合表达网络分析 (WGCNA) 来识别基因表达模块.
主要成果:
- Th17原始化和RV-16感染改变了BECs中的基因表达,影响了INTERFERON,MAP-KINASE和TNF信号通路,同时降低了Cilia和代谢模块.
- 在没有直接病毒感染的情况下,Th17细胞在与RV-16感染的BEC共同培养时表达了干扰素和病毒反应模块的增加.
- 在BEC中增加的干扰素信号和Th17细胞中的干扰素反应与更高的病毒载荷相关. 在RV-16感染后,IFN-α,IFN-γ和IL-1β的分泌增加.
结论:
- Th17淋巴细胞在患有喘的儿童的支气管上皮质中增强了表皮干扰素对RV-16感染的反应.
- 这种相互作用可能会导致呼吸道炎症和儿童喘病毒感染期间的疾病严重程度.
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