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化学暴露与肺泡巨噬细胞反应:“肺部防御机制在吸入性损伤中的作用”。

Chemical exposure and alveolar macrophages responses: 'the role of pulmonary defense mechanism in inhalation injuries'.

机构信息

Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Alinasab Hospital, Labratory Department, Iranian Social Security Organization (ISSO), Tabriz, Iran.

出版信息

BMJ Open Respir Res. 2023 Jul;10(1). doi: 10.1136/bmjresp-2022-001589.

DOI:10.1136/bmjresp-2022-001589
PMID:37479504
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10364189/
Abstract

Epidemiological and clinical studies have indicated an association between particulate matter (PM) exposure and acute and chronic pulmonary inflammation, which may be registered as increased mortality and morbidity. Despite the increasing evidence, the pathophysiology mechanism of these PMs is still not fully characterised. Pulmonary alveolar macrophages (PAMs), as a predominant cell in the lung, play a critically important role in these pathological mechanisms. Toxin exposure triggers events associated with macrophage activation, including oxidative stress, acute damage, tissue disruption, remodelling and fibrosis. Targeting macrophage may potentially be employed to treat these types of lung inflammation without affecting the natural immune response to bacterial infections. Biological toxins, their sources of exposure, physical and other properties, and their effects on the individuals are summarised in this article. Inhaled particulates from air pollution and toxic gases containing chemicals can interact with alveolar epithelial cells and immune cells in the airways. PAMs can sense ambient pollutants and be stimulated, triggering cellular signalling pathways. These cells are highly adaptable and can change their function and phenotype in response to inhaled agents. PAMs also have the ability to polarise and undergo plasticity in response to tissue damage, while maintaining resistance to exposure to inhaled agents.

摘要

流行病学和临床研究表明,颗粒物(PM)暴露与急性和慢性肺部炎症之间存在关联,这可能导致死亡率和发病率上升。尽管证据越来越多,但这些 PM 的病理生理学机制仍未完全阐明。肺泡巨噬细胞(PAMs)作为肺部的主要细胞,在这些病理机制中起着至关重要的作用。毒素暴露会引发与巨噬细胞激活相关的事件,包括氧化应激、急性损伤、组织破坏、重塑和纤维化。靶向巨噬细胞可能是治疗这些类型的肺部炎症而不影响对细菌感染的天然免疫反应的一种潜在方法。本文总结了生物毒素的来源、物理和其他特性,以及它们对个体的影响。空气污染中的吸入性颗粒物和含有化学物质的有毒气体可以与气道中的肺泡上皮细胞和免疫细胞相互作用。PAMs 可以感知环境污染物并被刺激,触发细胞信号通路。这些细胞具有高度的适应性,可以根据吸入剂的变化改变其功能和表型。PAMs 还能够在响应组织损伤时极化并发生可塑性,同时保持对吸入剂的抵抗力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/484a/10364189/2f2d3b17d314/bmjresp-2022-001589f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/484a/10364189/2f2d3b17d314/bmjresp-2022-001589f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/484a/10364189/2f2d3b17d314/bmjresp-2022-001589f01.jpg

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