ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Innate and ozone-induced airway hyperresponsiveness in obese mice: role of TNF-α.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Protective Effects of Ozone against Quinolinic Acid-Induced Redox Imbalance in Murine BV-2 Microglial Cells.Neurotoxicity research · 2026Article
- Hyaluronan Directs Alveolar Type II Cell Response to Acute Ozone Exposure in Mice.American journal of respiratory cell and molecular biology · 2025Article
- Role of body anthropometry in severe asthmatic patients: Evidences from the Severe Asthma Network in Italy (SANI) registry.The World Allergy Organization journal · 2025Article
- Younger severe asthma patients with interleukin 4 (CC variant) and dupilumab treatment are more likely to achieve clinical remission.BMC pulmonary medicine · 2025Article
- A Review onEndocrine, metabolic & immune disorders drug targets · 2025Review
- Weighted Breaths: Exploring Biologic and Non-Biologic Therapies for Co-Existing Asthma and Obesity.Current allergy and asthma reports · 2024Review
- Therapeutic ketosis decreases methacholine hyperresponsiveness in mouse models of inherent obese asthma.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma.Frontiers in immunology · 2021Review
- Obesity-Driven Deficiencies of Specialized Pro-resolving Mediators May Drive Adverse Outcomes During SARS-CoV-2 Infection.Frontiers in immunology · 2020Review
- Microbiota Contribute to Obesity-related Increases in the Pulmonary Response to Ozone.American journal of respiratory cell and molecular biology · 2019Article
- Sex Modifies Acute Ozone-Mediated Airway Physiologic Responses.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Beyond BMI: Obesity and Lung Disease.Chest · 2018Review
- Mechanistic Basis for Obesity-related Increases in Ozone-induced Airway Hyperresponsiveness in Mice.Annals of the American Thoracic Society · 2017Review
- Thermoneutral housing temperature regulates T-regulatory cell function and inhibits ovabumin-induced asthma development in mice.Scientific reports · 2017Article
- Saturated Fatty Acid Increases Lung Macrophages and Augments House Dust Mite-Induced Airway Inflammation in Mice Fed with High-Fat Diet.Inflammation · 2017Article
- IL-33 Drives Augmented Responses to Ozone in Obese Mice.Environmental health perspectives · 2017Article
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Hyaluronan mediates ozone-induced airway hyperresponsiveness in mice.The Journal of biological chemistry · 2016Article
- Hypoxia-induced pulmonary arterial hypertension augments lung injury and airway reactivity caused by ozone exposure.Toxicology and applied pharmacology · 2016Article
- A Comparative Study of Lung Host Defense in Murine Obesity Models. Insights into Neutrophil Function.American journal of respiratory cell and molecular biology · 2016Article
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Authors and funding
6 authors.
Funding
Abstract
Innate airway hyperresponsiveness (AHR) and augmented responses to ozone, an asthma trigger, are characteristics of obese mice. Systemic inflammation, a condition of increased circulating concentrations of inflammatory moieties, occurs in obesity. We hypothesized that TNF-α, via its effects as a master effector of this systemic inflammation, regulates innate AHR and augmented responses to ozone in obese mice. Therefore, we examined pulmonary inflammation and airway responsiveness in unexposed or ozone-exposed (2 ppm for 3 h) lean wild-type and obese Cpe(fat) mice that were TNF-α sufficient or deficient. Cpe(fat) mice lack carboxypeptidase E, which regulates satiety. Compared with wild type, Cpe(fat) mice had elevated serum IL-17A, G-CSF, KC, MCP-1, IL-9, MIG, and leptin, indicating systemic inflammation. Despite reductions in most of these moieties in TNF-α-deficient vs. -sufficient Cpe(fat) mice, we observed no substantial difference in airway responsiveness in these two groups of mice. Ozone-induced increases in bronchoalveolar lavage (BAL) neutrophils and macrophages were lower, but ozone-induced AHR and increases in BAL hyaluronan, osteopontin, IL-13, and protein carbonyls, a marker of oxidative stress, were augmented in TNF-α-deficient vs. -sufficient Cpe(fat) mice. Our data indicate that TNF-α has an important role in promoting the systemic inflammation but not the innate AHR of obesity, suggesting that the systemic inflammation of obesity is not the major driver of this AHR. TNF-α is required for the augmented effects of acute ozone exposure on pulmonary inflammatory cell recruitment in obese mice, whereas TNF-α protects against ozone-induced AHR in obese mice, possibly by suppressing ozone-induced oxidative stress.
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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.