Emerging Insights into the Impact of Air Pollution on Immune-Mediated Asthma Pathogenesis.

Emerging Insights into the Impact of Air Pollution on Immune-Mediated Asthma Pathogenesis.
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空气污染对免疫介导的哮喘发病机制的影响的新见解。

DOI:
10.1007/s11882-022-01034-1
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发表时间:
2022-07
影响因子:
5.5
通讯作者:
Gowdy, K. M.
Gowdy, K. M.
中科院分区:
医学2区
文献类型:
--
作者:
Tuazon, J. A.;Kilburg-Basnyat, B.;Oldfield, L. M.;Wiscovitch-Russo, R.;Dunigan-Russell, K.;Fedulov, A., V;Oestreich, K. J.;Gowdy, K. M.

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环境空气污染物水平的增加与肺部炎症和重塑有关,这些过程导致过敏性哮喘的发展和恶化。传统的研究主要集中在CD4+ T辅助细胞2(TH2)细胞在空气污染诱导的哮喘发病机制中的作用。然而,在过去十年中的许多工作已经发现了一系列空气污染诱导的非TH2免疫机制,这些机制有助于过敏性气道炎症和疾病。在本文中,我们回顾了当前的研究,证明了常见空气污染物及其对非TH 2免疫反应(包括PRR、ILC和非TH 2 T细胞亚群)的下游影响之间的联系,这些免疫反应是哮喘的关键参与者。我们还讨论了空气污染增加免疫介导的哮喘风险的拟议机制,包括预先存在的遗传风险,免疫细胞的表观遗传改变以及肺和肠道微生物组的组成和功能的干扰。总之,这些研究揭示了各种空气污染物通过遗传,表观遗传和基于微生物组的机制对先天和适应性免疫功能的多方面影响,这些机制促进了哮喘的诱导和恶化。
Increases in ambient levels of air pollutants have been linked to lung inflammation and remodeling, processes that lead to the development and exacerbation of allergic asthma. Conventional research has focused on the role of CD4+ T helper 2 (TH2) cells in the pathogenesis of air pollution-induced asthma. However, much work in the past decade has uncovered an array of air pollution-induced non-TH2 immune mechanisms that contribute to allergic airway inflammation and disease. In this article, we review current research demonstrating the connection between common air pollutants and their downstream effects on non-TH2 immune responses emerging as key players in asthma, including PRRs, ILCs, and non-TH2 T cell subsets. We also discuss the proposed mechanisms by which air pollution increases immune-mediated asthma risk, including pre-existing genetic risk, epigenetic alterations in immune cells, and perturbation of the composition and function of the lung and gut microbiomes. Together, these studies reveal the multifaceted impacts of various air pollutants on innate and adaptive immune functions via genetic, epigenetic, and microbiome-based mechanisms that facilitate the induction and worsening of asthma.
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