ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Endogenous osteopontin promotes ozone-induced neutrophil recruitment to the lungs and airway hyperresponsiveness to methacholine.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Osteopontin from monocyte-derived dendritic cells mediates ozone-induced pulmonary responses in mice.Frontiers in immunology · 2026Article
- Evaluating the role of alveolar macrophages in tolerance to ozone.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Transcriptional profiling of lung macrophages following ozone exposure in mice identifies signaling pathways regulating immunometabolic activation.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Relationships between Interleukin 18 -607 C/A and -137 G/C, Osteopontin -9250 C/T Genetic Polymorphisms and Systemic Inflammatory Response Syndrome in Coronary Artery Bypass Graft Surgery.Medicina (Kaunas, Lithuania) · 2024Article
- Inconsequential role for chemerin-like receptor 1 in the manifestation of ozone-induced lung pathophysiology in male mice.Physiological reports · 2024Article
- Interleukin-11 receptor subunit α-1 is required for maximal airway responsiveness to methacholine after acute exposure to ozone.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Epithelial microRNA-30a-3p targets RUNX2/HMGB1 axis to suppress airway eosinophilic inflammation in asthma.Respiratory research · 2022Article
- Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Androgens augment pulmonary responses to ozone in mice.Physiological reports · 2019Article
- Sex Modifies Acute Ozone-Mediated Airway Physiologic Responses.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- The Microbiome Regulates Pulmonary Responses to Ozone in Mice.American journal of respiratory cell and molecular biology · 2018Article
- Chemokine (C-C Motif) Receptor-Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone.Physiological reports · 2017Article
- Modulation of infection-mediated migration of neutrophils and CXCR2 trafficking by osteopontin.Immunology · 2017Article
- Plasminogen activator inhibitor-1 does not contribute to the pulmonary pathology induced by acute exposure to ozone.Physiological reports · 2016Article
- Regulation of IL-17A expression in mice following subacute ozone exposure.Journal of immunotoxicology · 2016Article
- Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- ROCK insufficiency attenuates ozone-induced airway hyperresponsiveness in mice.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Innate and ozone-induced airway hyperresponsiveness in obese mice: role of TNF-α.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Effect of antigen sensitization and challenge on oscillatory mechanics of the lung and pulmonary inflammation in obese carboxypeptidase E-deficient mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Inhalation of ozone (O₃), a common environmental pollutant, causes pulmonary injury, pulmonary inflammation, and airway hyperresponsiveness (AHR) in healthy individuals and exacerbates many of these same sequelae in individuals with preexisting lung disease. However, the mechanisms underlying these phenomena are poorly understood. Consequently, we sought to determine the contribution of osteopontin (OPN), a hormone and a pleiotropic cytokine, to the development of O₃-induced pulmonary injury, pulmonary inflammation, and AHR. To that end, we examined indices of these aforementioned sequelae in mice genetically deficient in OPN and in wild-type, C57BL/6 mice 24 h following the cessation of an acute (3 h) exposure to filtered room air (air) or O₃ (2 parts/million). In wild-type mice, O₃ exposure increased bronchoalveolar lavage fluid (BALF) OPN, whereas immunohistochemical analysis demonstrated that there were no differences in the number of OPN-positive alveolar macrophages between air- and O₃-exposed wild-type mice. O₃ exposure also increased BALF epithelial cells, protein, and neutrophils in wild-type and OPN-deficient mice compared with genotype-matched, air-exposed controls. However, following O₃ exposure, BALF neutrophils were significantly reduced in OPN-deficient compared with wild-type mice. When airway responsiveness to inhaled acetyl-β-methylcholine chloride (methacholine) was assessed using the forced oscillation technique, O₃ exposure caused hyperresponsiveness to methacholine in the airways and lung parenchyma of wild-type mice, but not OPN-deficient mice. These results demonstrate that OPN is increased in the air spaces following acute exposure to O₃ and functionally contributes to the development of O₃-induced pulmonary inflammation and airway and lung parenchymal hyperresponsiveness to methacholine.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.