title: Inflammatory cell signaling following exposures to particulate matter and ozone.
abstract: 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.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.affiliation: College of Public Health, Zhengzhou University, Zhengzhou, Henan Province 450001, PR China.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Yan
authors.affiliation: College of Public Health, Zhengzhou University, Zhengzhou, Henan Province 450001, PR China.
authors.forename: Yuefei
authors.initials: Y
authors.lastname: Jin
authors.affiliation: 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.
authors.forename: Zhen
authors.initials: Z
authors.lastname: An
authors.affiliation: 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.
authors.forename: Yingying
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, NC 27599, USA.
authors.forename: James M
authors.initials: JM
authors.lastname: Samet
authors.affiliation: 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.
authors.forename: Weidong
authors.initials: W
authors.lastname: Wu
mesh_terms: D056809:Alveolar Epithelial Cells / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D066246:ErbB Receptors / Q000235:genetics / Q000276:immunology; D005786:Gene Expression Regulation; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000276:immunology; D051267:NF-E2-Related Factor 2 / Q000235:genetics / Q000276:immunology; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D000070576:NLR Proteins / Q000235:genetics / Q000276:immunology; D010126:Ozone / Q000633:toxicity*; D052638:Particulate Matter / Q000633:toxicity*; D010710:Phosphates / Q000819:agonists / Q000276:immunology; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000276:immunology; D011014:Pneumonia / Q000209:etiology / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D017382:Reactive Oxygen Species / Q000819:agonists / Q000276:immunology; D015398:Signal Transduction / Q000187:drug effects*; D051193:Toll-Like Receptors / Q000235:genetics / Q000276:immunology
chemical_list: D051267:NF-E2-Related Factor 2; D016328:NF-kappa B; C495635:NFE2L2 protein, human; D000070576:NLR Proteins; D052638:Particulate Matter; D010710:Phosphates; D017382:Reactive Oxygen Species; D051193:Toll-Like Receptors; D010126:Ozone; D019869:Phosphatidylinositol 3-Kinases; D066246:ErbB Receptors; D020928:Mitogen-Activated Protein Kinases
keywords: Cell signaling; Inflammation; O(3); Particulate matter