Ozone impairs endogenous compensatory responses in allergic asthma.

Autor: Ho K; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Weimar D; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Torres-Matias G; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America; Biomedical Sciences Graduate Program, The Ohio State University, Columbus, OH, United States of America., Lee H; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Shamsi S; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Shalosky E; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Yaeger M; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America; Biomedical Sciences Graduate Program, The Ohio State University, Columbus, OH, United States of America., Hartzler-Lovins H; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America; Molecular, Cellular and Developmental Biology Graduate Program, The Ohio State University, Columbus, OH, United States of America., Dunigan-Russell K; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Jelic D; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Novak CM; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Gowdy KM; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Englert JA; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America., Ballinger MN; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, OH, United States of America. Electronic address: megan.ballinger@osumc.edu.
Jazyk: angličtina
Zdroj: Toxicology and applied pharmacology [Toxicol Appl Pharmacol] 2023 Jan 15; Vol. 459, pp. 116341. Date of Electronic Publication: 2022 Dec 08.
DOI: 10.1016/j.taap.2022.116341
Abstrakt: Asthma is a chronic inflammatory airway disease characterized by acute exacerbations triggered by inhaled allergens, respiratory infections, or air pollution. Ozone (O 3 ), a major component of air pollution, can damage the lung epithelium in healthy individuals. Despite this association, little is known about the effects of O 3 and its impact on chronic lung disease. Epidemiological data have demonstrated that elevations in ambient O 3 are associated with increased asthma exacerbations. To identify mechanisms by which O 3 exposure leads to asthma exacerbations, we developed a two-hit mouse model where mice were sensitized and challenged with three common allergens (dust mite, ragweed and Aspergillus fumigates, DRA) to induce allergic inflammation prior to exposure to O 3 (DRAO 3 ). Changes in lung physiology, inflammatory cells, and inflammation were measured. Exposure to O 3 following DRA significantly increased airway hyperreactivity (AHR), which was independent of TLR4. DRA exposure resulted in increased BAL eosinophilia while O 3 exposure resulted in neutrophilia. Additionally, O 3 exposure following DRA blunted anti-inflammatory and antioxidant responses. Finally, there were significantly less monocytes and innate lymphoid type 2 cells (ILC2s) in the dual challenged DRA-O 3 group suggesting that the lack of these immune cells may influence O 3 -induced AHR in the setting of allergic inflammation. In summary, we developed a mouse model that mirrors some aspects of the clinical course of asthma exacerbations due to air pollution and identified that O 3 exposure in the asthmatic lung leads to impaired endogenous anti-inflammatory and antioxidant responses and alterations inflammatory cell populations.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2022. Published by Elsevier Inc.)
Databáze: MEDLINE
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