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皮质可塑性和先天免疫激活促进呼吸道病毒感染后的肺组织重塑

Andrew K Beppu^1,2,3, Juanjuan Zhao^1,2,3, Changfu Yao^1,2,3

¹Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.

Nature communications

|September 19, 2023

概括

在流感感染后,肺部分泌细胞转化为基底细胞 (BCs),以修复气膜. 然而,这种修复过程并不能完全恢复小鼠的正常气体交换功能.

科学领域:

肺部医学肺部医学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

在干细胞枯竭后,小鼠肺部上皮质可塑性尚不清楚.
病毒感染和慢性肺部疾病导致干细胞丧失,气道基底细胞 (BC) 增生和免疫激活,导致肺重塑和功能障碍.

研究的目的:

调查表皮质可塑性在病毒感染后肺部修复中的作用.
确定参与肺再生的特定细胞类型及其功能结果.

主要方法:

使用了一种流感病毒感染的小鼠模型.
分析了肺上皮的细胞变化,重点关注基底细胞 (BCs) 和内血清 (IS) 细胞.
研究了IL-22信号在BC扩张和分化中的作用.

主要成果:

流感感染激活了远距离气道分泌细胞 (IS细胞) 的子集,以采用BC命运.
受伤诱导的超塑性BCs (hBCs) 表达了高水平的IL-22Ra1并以依赖IL-22的方式扩大.
炎症的解消导致重新填充的大气泡中的BC重新分化为IS细胞,增加了抗菌因子,但未能恢复正常的气泡气体交换.

结论:

远距离呼吸道分泌细胞可以在病毒性肺损伤期间充当基底细胞的原始细胞.
IL-22信号驱动这些原生细胞的扩张,以进行膜修复.
虽然促进了抗微生物防御,但这种再生过程并不能完全恢复膜上皮的气体交换功能.

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