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颗粒物空气污染如何影响肺血管内皮的屏障功能和炎症活性?

How does particulate air pollution affect barrier functions and inflammatory activity of lung vascular endothelium?

机构信息

Department of Immunology and Allergy, Chair of Pulmonology, Rheumatology and Clinical Immunology, Medical University of Lodz, Lodz, Poland.

出版信息

Allergy. 2023 Mar;78(3):629-638. doi: 10.1111/all.15630. Epub 2023 Jan 18.

DOI:10.1111/all.15630
PMID:36588285
Abstract

Both particulate matter and gaseous components of air pollution have already been shown to increase cardiovascular mortality in numerous studies. It is, however, important to note that on their way to the bloodstream the polluting agents pass the lung barrier. Inside the alveoli, particles of approximately 0.4-1 μm are most efficiently deposited and commonly undergo phagocytosis by lung macrophages. Not only the soluble agents, but also particles fine enough to leave the alveoli enter the bloodstream in this finite part of the endothelium, reaching thus higher concentrations in close proximity of the alveoli and endothelium. Additionally, deposits of particulate matter linger in direct proximity of the endothelial cells and may induce inflammation, immune responses, and influence endothelial barrier dysfunction thus increasing PM bioavailability in positive feedback. The presented discussion provides an overview of possible components of indoor PM and how endothelium is thus influenced, with emphasis on lung vascular endothelium and clinical perspectives.

摘要

已有大量研究表明,空气污染中的颗粒物和气体成分都会增加心血管疾病的死亡率。然而,值得注意的是,在进入血液的过程中,污染物质会穿过肺部屏障。在肺泡内,粒径约为 0.4-1 μm 的颗粒物质最容易沉积,并通常被肺巨噬细胞吞噬。不仅是可溶性物质,而且粒径小到足以离开肺泡的颗粒物质也会通过这部分有限的内皮细胞进入血液,从而在肺泡和内皮细胞附近达到更高的浓度。此外,颗粒物的沉积会在靠近内皮细胞的地方停留,并可能引发炎症、免疫反应,影响内皮细胞屏障功能,从而通过正反馈增加 PM 的生物利用度。本文综述了室内 PM 的可能成分,以及它们是如何影响内皮细胞的,重点关注肺血管内皮细胞和临床观点。

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