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在慢性肺损伤中纤维细胞和单细胞衍生细胞之间的相互作用,这些损伤是由真实环境中的颗粒物暴露引起的

Youjin Zeng¹, Rui Zhang¹, Yue Jiang¹

¹Department of Toxicology, Guangdong Provincial Key Laboratory of Food, Nutrition and Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.

Mutation research. Genetic toxicology and environmental mutagenesis

|September 26, 2024

概括

长期暴露于细颗粒物 (PM2.5) 改变了肺介质细胞,增加了亲炎性和亲纤维性亚型. 这创造了一个可能导致肺纤维化和癌症发展的环境.

科学领域:

环境健康环境健康
肺部医学肺部医学
免疫学免疫学免疫学

背景情况:

长期暴露于细颗粒物 (PM2.5) 与慢性肺部疾病有关,包括炎症,纤维化和癌症.
像纤维细胞和骨髓衍生抑制细胞 (MDSC) 这样的介质细胞对于肺免疫调节至关重要,但它们在PM引起的损伤中的作用尚未完全理解.

研究的目的:

研究长期真实环境中对介质细胞多样性和小鼠肺部功能的长期PM暴露的影响.
描述慢性PM暴露后肺组织中的细胞和分子变化.

主要方法:

一项为期16周的暴露实验,使用C57BL/6J雄性小鼠的真实环境PM.
单细胞RNA测序 (scRNA-seq) 分析肺组织以确定细胞和分子变化.

主要成果:

观察到特定纤维细胞亚群 (ATX +,Col5a1 + Meg3 +,通用纤维细胞) 和单细胞衍生细胞 (单细胞-MDSC,特定间歇性巨细胞亚型) 的显着增加.
这些已识别的细胞亚群表现出亲炎性和亲纤维性功能.
该研究揭示了免疫抑制信号通路和细胞因子相互作用,创造了一个类似于癌症相关纤维细胞 (CAF) 和瘤相关巨细胞 (TAM) 的肺微环境.

结论:

长期暴露于PM2.5会促进肺部特定的亲炎性和亲纤维性介质细胞亚群的扩张.
这些细胞变化有助于改变免疫微环境,可能促进PM诱导的肺纤维化和癌症.
介质细胞在由颗粒物诱导的慢性肺损伤的病原发生中发挥着关键作用.

关键词:

致癌途径致癌途径慢性肺损伤是一种慢性肺损伤.纤维细胞的细胞.微细颗粒物质的细颗粒物质的细颗粒物质的细颗粒物质的细颗粒物质.免疫抑制是一种免疫抑制.单细胞衍生细胞是单细胞衍生细胞.

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