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哮喘患者气道高敏反应及对吸入二氧化硫反应的机制

Mechanisms of Heightened Airway Sensitivity and Responses to Inhaled SO2 in Asthmatics.

作者信息

Reno Anita L, Brooks Edward G, Ameredes Bill T

机构信息

University of Texas Medical Branch, Texas, USA.

University of Texas Health Science Center at San Antonio, Texas, USA.

出版信息

Environ Health Insights. 2015 Apr 1;9(Suppl 1):13-25. doi: 10.4137/EHI.S15671. eCollection 2015.

Abstract

Sulfur dioxide (SO2) is a problematic inhalable air pollutant in areas of widespread industrialization, not only in the United States but also in countries undergoing rapid industrialization, such as China, and it can be a potential trigger factor for asthma exacerbations. It is known that asthmatics are sensitive to the effects of SO2; however, the basis of this enhanced sensitivity remains incompletely understood. A PubMed search was performed over the course of 2014, encompassing the following terms: asthma, airway inflammation, sulfur dioxide, IL-10, mouse studies, and human studies. This search indicated that biomarkers of SO2 exposure, SO2 effects on airway epithelial cell function, and animal model data are useful in our understanding of the body's response to SO2, as are SO2-associated amplification of allergic inflammation, and potential promotion of neurogenic inflammation due to chemical irritant properties. While definitive answers are still being sought, these areas comprise important foci of consideration regarding asthmatic responses to inhaled SO2. Furthermore, IL-10 deficiency associated with asthma may be another important factor associated with an inability to resolve inflammation and mitigate oxidative stress resulting from SO2 inhalation, supporting the idea that asthmatics are predisposed to SO2 sensitivity, leading to asthma exacerbations and airway dysfunction.

摘要

二氧化硫(SO₂)是广泛工业化地区存在问题的可吸入空气污染物,不仅在美国如此,在正经历快速工业化的国家如中国也是如此,并且它可能是哮喘发作的潜在触发因素。已知哮喘患者对SO₂的影响敏感;然而,这种增强敏感性的基础仍未完全理解。在2014年期间进行了一次PubMed搜索,涵盖以下术语:哮喘、气道炎症、二氧化硫、白细胞介素-10、小鼠研究和人体研究。该搜索表明,SO₂暴露的生物标志物、SO₂对气道上皮细胞功能的影响以及动物模型数据,对于我们理解人体对SO₂的反应很有用,SO₂相关的过敏性炎症放大以及由于化学刺激特性可能促进神经源性炎症也是如此。虽然仍在寻求确切答案,但这些领域是关于哮喘患者对吸入SO₂反应的重要考虑焦点。此外,与哮喘相关的白细胞介素-10缺乏可能是另一个与无法解决炎症和减轻吸入SO₂导致的氧化应激相关的重要因素,支持了哮喘患者易对SO₂敏感的观点,并导致哮喘发作和气道功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2230/4384764/e14b64b6ec58/ehi-suppl.1-2015-013f1.jpg

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