J A Tuazon1,2, B Kilburg-Basnyat3, L M Oldfield4,5, R Wiscovitch-Russo4, K Dunigan-Russell6, A V Fedulov7, K J Oestreich1,8, K M Gowdy9. 1. Department of Microbial Infection and Immunity, The Ohio State University Wexner Medical Center, Columbus, OH, 43210, USA. 2. Medical Scientist Training Program, The Ohio State University, Columbus, OH, 43210, USA. 3. Department of Pharmacology and Toxicology, East Carolina University, Greenville, NC, 27858, USA. 4. Department of Synthetic Biology and Bioenergy, J. Craig Venter Institute, Rockville, MD, 20850, USA. 5. Department of Synthetic Genomics, Replay Holdings LLC, San Diego, 92121, USA. 6. Division of Pulmonary, Critical Care, and Sleep Medicine, The Ohio State University Wexner Medical Center, Davis Heart and Lung Research Institute, Columbus, OH, 43210, USA. 7. Division of Surgical Research, Department of Surgery, Alpert Medical School, Brown University, Rhode Island Hospital, Providence, RI, 02903, USA. 8. Pelotonia Institute for Immuno-Oncology, The Ohio State University, The James Comprehensive Cancer Center, Columbus, OH, 43210, USA. 9. Division of Pulmonary, Critical Care, and Sleep Medicine, The Ohio State University Wexner Medical Center, Davis Heart and Lung Research Institute, Columbus, OH, 43210, USA. kymberly.gowdy@osumc.edu.
Abstract
PURPOSE OF REVIEW: Increases in ambient levels of air pollutants have been linked to lung inflammation and remodeling, processes that lead to the development and exacerbation of allergic asthma. Conventional research has focused on the role of CD4+ T helper 2 (TH2) cells in the pathogenesis of air pollution-induced asthma. However, much work in the past decade has uncovered an array of air pollution-induced non-TH2 immune mechanisms that contribute to allergic airway inflammation and disease. RECENT FINDINGS: In this article, we review current research demonstrating the connection between common air pollutants and their downstream effects on non-TH2 immune responses emerging as key players in asthma, including PRRs, ILCs, and non-TH2 T cell subsets. We also discuss the proposed mechanisms by which air pollution increases immune-mediated asthma risk, including pre-existing genetic risk, epigenetic alterations in immune cells, and perturbation of the composition and function of the lung and gut microbiomes. Together, these studies reveal the multifaceted impacts of various air pollutants on innate and adaptive immune functions via genetic, epigenetic, and microbiome-based mechanisms that facilitate the induction and worsening of asthma.
PURPOSE OF REVIEW: Increases in ambient levels of air pollutants have been linked to lung inflammation and remodeling, processes that lead to the development and exacerbation of allergic asthma. Conventional research has focused on the role of CD4+ T helper 2 (TH2) cells in the pathogenesis of air pollution-induced asthma. However, much work in the past decade has uncovered an array of air pollution-induced non-TH2 immune mechanisms that contribute to allergic airway inflammation and disease. RECENT FINDINGS: In this article, we review current research demonstrating the connection between common air pollutants and their downstream effects on non-TH2 immune responses emerging as key players in asthma, including PRRs, ILCs, and non-TH2 T cell subsets. We also discuss the proposed mechanisms by which air pollution increases immune-mediated asthma risk, including pre-existing genetic risk, epigenetic alterations in immune cells, and perturbation of the composition and function of the lung and gut microbiomes. Together, these studies reveal the multifaceted impacts of various air pollutants on innate and adaptive immune functions via genetic, epigenetic, and microbiome-based mechanisms that facilitate the induction and worsening of asthma.
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