Inflammatory cell signaling following exposures to particulate matter and ozone

• Published in: Biochimica et biophysica acta Vol. 1860; no. 12; pp. 2826 - 2834
• Main Authors: Yan, Zhen, Jin, Yuefei, An, Zhen, Liu, Yingying, Samet, James M., Wu, Weidong
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.12.2016
• Subjects: adverse effects; air; air pollution; Alveolar Epithelial Cells - drug effects; Alveolar Epithelial Cells - immunology; Alveolar Epithelial Cells - pathology; antioxidants; Cell signaling; epidermal growth factor receptors; Gene Expression Regulation; Humans; Inflammation; intracellular signaling peptides and proteins; mitogen-activated protein kinase kinase; Mitogen-Activated Protein Kinases - genetics; Mitogen-Activated Protein Kinases - immunology; NF-E2-Related Factor 2 - genetics; NF-E2-Related Factor 2 - immunology; NF-kappa B - genetics; NF-kappa B - immunology; NLR Proteins - genetics; NLR Proteins - immunology; ozone; Ozone - toxicity; Particulate matter; Particulate Matter - toxicity; particulates; pathogenesis; phosphates; Phosphates - agonists; Phosphates - immunology; phosphatidylinositol 3-kinase; Phosphatidylinositol 3-Kinases - genetics; Phosphatidylinositol 3-Kinases - immunology; Pneumonia - etiology; Pneumonia - genetics; Pneumonia - immunology; Pneumonia - pathology; pollutants; Reactive Oxygen Species - agonists; Reactive Oxygen Species - immunology; Receptor, Epidermal Growth Factor - genetics; Receptor, Epidermal Growth Factor - immunology; respiratory tract diseases; signal transduction; Signal Transduction - drug effects; Toll-Like Receptors - genetics; Toll-Like Receptors - immunology; toxicity; transcription factor NF-kappa B; CXCL; HB-EGF; NLRCs; ICAM-1; AHR; AP-1; MyD88; NF-κB; PI3K; NLRPs; PAMPs; PM2.5–10; ROFA; MAPKs; VOCs; NOD; IL; TACE; GPx; MAPKKK; TGF; ARE; ROS; UGT1a6; ERK; O3; COX-2; PRRs; MAPKK; HO-1; PTP; EGFR; LPS; Cell signaling; DAMPs; c-Src; Nrf2; NOx; GPCRs; PM2.5; PM0.1; 8-OHdG; NQO1; EGF; GST; SOD; Inflammation; Akt; DEP; VCAM-1; TNF-α; GCS; MKP-1; Particulate matter; PAHs; HA; PM; TLRs; COPD; O
• ISSN: 0304-4165; 0006-3002; 1872-8006
• DOI: 10.1016/j.bbagen.2016.03.030

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. •Exposure to PM or O3 can activate cellular signaling networks that regulate inflammatory responses.•While PM-induced cell signaling is associated with resultant ROS, O3-induced cell signaling implicates phosphates.•The cellular signaling induced by PM and O3 exposure varies with cell type and physiochemical properties of these pollutants.