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气道高反应性的发展与 PM2.5 的毒性

Airway hyperresponsiveness development and the toxicity of PM2.5.

机构信息

Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei Province, China.

Department of Central Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei Province, China.

出版信息

Environ Sci Pollut Res Int. 2021 Feb;28(6):6374-6391. doi: 10.1007/s11356-020-12051-w. Epub 2021 Jan 4.

DOI:10.1007/s11356-020-12051-w
PMID:33394441
Abstract

Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and increased airway resistance. AHR is recognized as a key characteristic of asthma and is associated with significant morbidity. At present, many studies on the molecular mechanisms of AHR have mainly focused on the imbalance in Th1/Th2 cell function and the abnormal contraction of airway smooth muscle cells. However, the specific mechanisms of AHR remain unclear and need to be systematically elaborated. In addition, the effect of air pollution on the respiratory system has become a worldwide concern. To date, numerous studies have indicated that certain concentrations of fine particulate matter (PM2.5) can increase airway responsiveness and induce acute exacerbation of asthma. Of note, the concentration of PM2.5 does correlate with the degree of AHR. Numerous studies exploring the toxicity of PM2.5 have mainly focused on the inflammatory response, oxidative stress, genotoxicity, apoptosis, autophagy, and so on. However, there have been few reviews systematically elaborating the molecular mechanisms by which PM2.5 induces AHR. The present review separately sheds light on the underlying molecular mechanisms of AHR and PM2.5-induced AHR.

摘要

气道高反应性(AHR)的特征是对非特异性刺激过度的支气管收缩,从而导致气道狭窄和气道阻力增加。AHR 被认为是哮喘的一个关键特征,并与显著的发病率相关。目前,许多关于 AHR 分子机制的研究主要集中在 Th1/Th2 细胞功能失衡和气道平滑肌细胞异常收缩上。然而,AHR 的具体机制仍不清楚,需要系统地阐述。此外,空气污染对呼吸系统的影响已成为全球关注的焦点。迄今为止,大量研究表明,一定浓度的细颗粒物(PM2.5)可以增加气道反应性并诱发哮喘急性加重。值得注意的是,PM2.5 的浓度与 AHR 的程度相关。许多研究 PM2.5 毒性的主要集中在炎症反应、氧化应激、遗传毒性、细胞凋亡、自噬等方面。然而,很少有综述系统地阐述了 PM2.5 诱导 AHR 的分子机制。本综述分别阐述了 AHR 和 PM2.5 诱导的 AHR 的潜在分子机制。

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