TRP通道和交通相关的环境污染引起的肺疾病
2016/07/28
摘要
环境污染物暴露是不良健康结果的主要危险因素，导致人类的发病率和死亡率增加。柴油废气（DE）是交通相关空气污染的主要有害成分之一。暴露在柴油废气中会影响包括呼吸道的很多生理系统，肺部疾病在这些人口密集的城市地区不断增加。因此，迫切需要（1）创造更新更少污染的燃料，（2）改善排气后处理和减少排放，（3）了解常规燃料和清洁柴油燃料对肺部的毒性作用机制。这些步骤可能有助于诊断和干预措施的发展，以防止与交通有关的空气污染对肺系统的负面影响。废气从常规燃料到较小程度的清洁燃料，包含颗粒物（PM）和超过400个额外的化学成分。主要的有毒成分是氮氧化物（NOx）和多环芳香烃（PAHs）。颗粒物和多环芳烃可能通过瞬时受体电位（TRP）通道发挥潜在作用。在这篇综述中，我们首先讨论了从传统的柴油废气和清洁燃料技术与急性和慢性气道炎症之间的关联。我们将审查颗粒物和多环芳烃可能激活和/或增强TRP辣椒素1型（TRPV1）和锚蛋白1（TRPA1）通道。最后，我们将讨论和总结最近机制研究的结果，TRPs可以控制柴油废气和气道炎症之间的联系，这是一个导致肺部疾病的主要因素。
（杨冬 审校）
Semin Immunopathol. 2016 May;38(3):331-8. doi: 10.1007/s00281-016-0554-4. Epub 2016 Feb 2.
TRP channels and traffic-related environmental pollution-induced pulmonary disease.
Akopian AN1, Fanick ER2, Brooks EG3,4.
Author information
Abstract
Environmental pollutant exposures are major risk factors for adverse health outcomes, with increased morbidity and mortality in humans. Diesel exhaust (DE) is one of the major harmful components of traffic-related air pollution. Exposure to DE affects several physiological systems, including the airways, and pulmonary diseases are increased in highly populated urban areas. Hence, there are urgent needs to (1) create newer and lesser polluting fuels, (2) improve exhaust aftertreatments and reduce emissions, and (3) understand mechanisms of actions for toxic effects of both conventional and cleaner diesel fuels on the lungs. These steps could aid the development of diagnostics and interventions to prevent the negative impact of traffic-related air pollution on the pulmonary system. Exhaust from conventional, and to a lesser extent, clean fuels, contains particulate matter (PM) and more than 400 additional chemical constituents. The major toxic constituents are nitrogen oxides (NOx) and polycyclic aromatic hydrocarbons (PAHs). PM and PAHs could potentially act via transient receptor potential (TRP) channels. In this review, we will first discuss the associations between DE from conventional as well as clean fuel technologies and acute and chronic airway inflammation. We will then review possible activation and/or potentiation of TRP vanilloid type 1 (TRPV1) and ankyrin 1 (TRPA1) channels by PM and PAHs. Finally, we will discuss and summarize recent findings on the mechanisms whereby TRPs could control the link between DE and airway inflammation, which is a primary determinant leading to pulmonary disease.
KEYWORDS:Acute lung injury; Asthma; Clean diesel; Diesel exhaust particles (DEP); Polycyclic aromatic hydrocarbons (PAHs); TRPA1; TRPV1
Semin Immunopathol. 2016 May;38(3):331-8. doi: 10.1007/s00281-016-0554-4. Epub 2016 Feb 2.
