粗颗粒物 (PM10) 通过NLRP3激活诱导炎症反应
Damariz Marín-Palma1,2, Jorge H Tabares-Guevara2, Natalia Taborda3
1Infettare, Facultad de Medicina, Universidad Cooperativa de Colombia, Medellín, Colombia.
Journal of inflammation (London, England)
|May 2, 2024
概括
颗粒物 (PM10) 暴露会损害细胞活力并引发炎症,激活NLRP3炎症酶并增加IL-1β的产生. 肺部的这种反应可能会使呼吸道状况恶化.
科学领域:
- 环境毒理学环境毒理学
- 免疫学 免疫学 免疫学
- 呼吸系统药物 呼吸系统药物
背景情况:
- 颗粒物暴露与炎症和氧化应激有关,其影响因化学成分和大小而异.
- 包括NLRP3炎症酶激活在内的PM10诱导炎症的特定机制需要进一步研究.
研究的目的:
- 用体外和体外模型评估PM10对细胞细胞毒性和炎症反应的影响.
- 探索NLRP3炎症酶激活在PM10诱导的炎症中的作用.
主要方法:
- 在体外:暴露于PM10的人类外周血液单核细胞 (PBMCs);评估了细胞毒性 (LDH测定),炎症组分表达 (qPCR),促炎细胞因子产生 (ELISA) 和ASC复合体形成 (聚焦显微镜).
- 在体内:被鼻内暴露于PM10的小鼠;分析了支气管支气管洗液的细胞计数和细胞因子水平 (ELISA),并在肺组织中量化了炎症基因表达 (qPCR).
主要成果:
- 在PM10的度>100μg/mL时,PM10在PBMC中诱导显著的细胞毒性.
- 暴露于PM10上调了促炎细胞因子 (特别是IL-1β) 和PBMC中ASC复合体的形成.
- 在小鼠中,PM10增加了肺免疫细胞 (多态核细胞) 的招募,并提高了肺组织中NLRP3,IL-1β和IL-18的表达.
结论:
- 暴露于PM10会降低初级细胞活力,并启动一种炎症级联,包括NLRP3炎症酶激活和IL-1β释放.
- PM10触发肺细胞招募和细胞因子表达,可能导致上皮损伤并加剧病毒感染等呼吸道疾病.
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