ArticleEnvironmental health perspectives2013
Augmented pulmonary responses to acute ozone exposure in obese mice: roles of TNFR2 and IL-13.
Article in Environmental health perspectives, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- A Review onEndocrine, metabolic & immune disorders drug targets · 2025Review
- Transcriptomics Underlying Pulmonary Ozone Pathogenesis Regulated by Inflammatory Mediators in Mice.Antioxidants (Basel, Switzerland) · 2021Article
- IL-33, diet-induced obesity, and pulmonary responses to ozone.Respiratory research · 2020Article
- Microbiota Contribute to Obesity-related Increases in the Pulmonary Response to Ozone.American journal of respiratory cell and molecular biology · 2019Article
- The influence of maternal and perinatal high-fat diet on ozone-induced pulmonary responses in offspring.Journal of toxicology and environmental health. Part A · 2019Article
- The Metabolic Response to Ozone.Frontiers in immunology · 2019Review
- Augmented Responses to Ozone in Obese Mice Require IL-17A and Gastrin-Releasing Peptide.American journal of respiratory cell and molecular biology · 2018Article
- Late-onset asthma: current perspectives.Journal of asthma and allergy · 2018Review
- Mechanistic Basis for Obesity-related Increases in Ozone-induced Airway Hyperresponsiveness in Mice.Annals of the American Thoracic Society · 2017Review
- Ozone Exposure, Cardiopulmonary Health, and Obesity: A Substantive Review.Chemical research in toxicology · 2017Review
- IL-33 Drives Augmented Responses to Ozone in Obese Mice.Environmental health perspectives · 2017Article
- Article
- Obesity, Asthma, and the Microbiome.Physiology (Bethesda, Md.) · 2016Review
- The administration of a high refined carbohydrate diet promoted an increase in pulmonary inflammation and oxidative stress in mice exposed to cigarette smoke.International journal of chronic obstructive pulmonary disease · 2016Article
- 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
- γδ T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice.PloS one · 2015Article
- Pivotal role of IL-6 in the hyperinflammatory responses to subacute ozone in adiponectin-deficient mice.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Ozone inhalation modifies the rat liver proteome.Redox biology · 2014Article
- γδ T cells are required for pulmonary IL-17A expression after ozone exposure in mice: role of TNFα.PloS one · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAcute ozone (O(3)) exposure results in greater inflammation and airway hyperresponsiveness (AHR) in obese versus lean mice.
objectivesWe examined the hypothesis that these augmented responses to O(3) are the result of greater signaling through tumor necrosis factor receptor 2 (TNFR2) and/or interleukin (IL)-13.
methodsWe exposed lean wild-type (WT) and TNFR2-deficient (TNFR2(-/-)) mice, and obese Cpe(fat) and TNFR2-deficient Cpe(fat) mice (Cpe(fat)/TNFR2(-/-)), to O(3) (2 ppm for 3 hr) either with or without treatment with anti-IL-13 or left them unexposed.
resultsO(3)-induced increases in baseline pulmonary mechanics, airway responsiveness, and cellular inflammation were greater in Cpe(fat) than in WT mice. In lean mice, TNFR2 deficiency ablated O(3)-induced AHR without affecting pulmonary inflammation; whereas in obese mice, TNFR2 deficiency augmented O(3)-induced AHR but reduced inflammatory cell recruitment. O(3) increased pulmonary expression of IL-13 in Cpe(fat) but not WT mice. Flow cytometry analysis of lung cells indicated greater IL-13-expressing CD(4+) cells in Cpe(fat) versus WT mice after O(3) exposure. In Cpe(fat) mice, anti-IL-13 treatment attenuated O(3)-induced increases in pulmonary mechanics and inflammatory cell recruitment, but did not affect AHR. These effects of anti-IL-13 treatment were not observed in Cpe(fat)/TNFR2(-/-) mice. There was no effect of anti-IL-13 treatment in WT mice.
conclusionsPulmonary responses to O(3) are not just greater, but qualitatively different, in obese versus lean mice. In particular, in obese mice, O(3) induces IL-13 and IL-13 synergizes with TNF via TNFR2 to exacerbate O(3)-induced changes in pulmonary mechanics and inflammatory cell recruitment but not AHR.
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