Zhen Yan1, Yuefei Jin1, Zhen An2, Yingying Liu2, James M Samet3, Weidong Wu4. 1. College of Public Health, Zhengzhou University, Zhengzhou, Henan Province 450001, PR China. 2. School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, PR China; Xinxiang Key Laboratory of Environmental Effects and Intervention, Xinxiang Medical University, Xinxiang, Henan Province 453003, PR China. 3. Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, NC 27599, USA. 4. School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, PR China; Xinxiang Key Laboratory of Environmental Effects and Intervention, Xinxiang Medical University, Xinxiang, Henan Province 453003, PR China; Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang, Henan Province 453003, PR China. Electronic address: wdwu2013@126.com.
Abstract
BACKGROUND: Particulate matter (PM) and ozone (O3) are two major ambient air pollutants. Epidemiological and toxicological studies have demonstrated exposure to these pollutants is associated with a variety of adverse health effects, including cardiovascular and respiratory disease, in which inflammation is believed to be a common and essential factor. SCOPE OF REVIEW: This review mainly focuses on major inflammatory cell signaling pathways triggered by exposure to PM and O3. The receptors covered in this review include the EGF receptor, toll like receptor, and NOD-like receptor. Intracellular signaling protein kinases depicted in this review are phosphatidylinositol 3-kinase and mitogen-activated protein kinases. Activation of antioxidant and inflammatory transcription factors such as NrF2 and NFκB induced by PM and O3 is also discussed. MAJOR CONCLUSIONS: Exposure to PM or O3 can activate cellular signaling networks including membrane receptors, intracellular kinases and phosphatases, and transcription factors that regulate inflammatory responses. While PM-induced cell signaling is associated with resultant ROS, O3-induced cell signaling implicates phosphates. Notably, the cellular signaling induced by PM and O3 exposure varies with cell type and physiochemical properties of these pollutants. GENERAL SIGNIFICANCE: Cellular signaling plays a critical role in the regulation of inflammatory pathogenesis. Elucidation of cellular signaling pathways initiated by PM or O3 cannot only help to uncover the mechanisms of air pollutant toxicity but also provide clues for development of interventional measures against air pollution-induced disorders. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
BACKGROUND: Particulate matter (PM) and ozone (O3) are two major ambient air pollutants. Epidemiological and toxicological studies have demonstrated exposure to these pollutants is associated with a variety of adverse health effects, including cardiovascular and respiratory disease, in which inflammation is believed to be a common and essential factor. SCOPE OF REVIEW: This review mainly focuses on major inflammatory cell signaling pathways triggered by exposure to PM and O3. The receptors covered in this review include the EGF receptor, toll like receptor, and NOD-like receptor. Intracellular signaling protein kinases depicted in this review are phosphatidylinositol 3-kinase and mitogen-activated protein kinases. Activation of antioxidant and inflammatory transcription factors such as NrF2 and NFκB induced by PM and O3 is also discussed. MAJOR CONCLUSIONS: Exposure to PM or O3 can activate cellular signaling networks including membrane receptors, intracellular kinases and phosphatases, and transcription factors that regulate inflammatory responses. While PM-induced cell signaling is associated with resultant ROS, O3-induced cell signaling implicates phosphates. Notably, the cellular signaling induced by PM and O3 exposure varies with cell type and physiochemical properties of these pollutants. GENERAL SIGNIFICANCE: Cellular signaling plays a critical role in the regulation of inflammatory pathogenesis. Elucidation of cellular signaling pathways initiated by PM or O3 cannot only help to uncover the mechanisms of air pollutant toxicity but also provide clues for development of interventional measures against air pollution-induced disorders. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
Authors: Kristina Shkirkova; Krista Lamorie-Foote; Michelle Connor; Arati Patel; Giuseppe Barisano; Hans Baertsch; Qinghai Liu; Todd E Morgan; Constantinos Sioutas; William J Mack Journal: J Toxicol Environ Health B Crit Rev Date: 2020-09-24 Impact factor: 6.393