ArticlePulmonary pharmacology & therapeutics2013
Obesity and airway responsiveness: role of TNFR2.
Article in Pulmonary pharmacology & therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Inflammatory Dysregulation, Asthma, and Obesity in Children: What is the Relationship?Journal of inflammation research · 2026Review
- A Review onEndocrine, metabolic & immune disorders drug targets · 2025Review
- A clinician's guide to effects of obesity on childhood asthma and into adulthood.Expert review of respiratory medicine · 2024Review
- Obesity Enhances Non-Th2 Airway Inflammation in a Murine Model of Allergic Asthma.International journal of molecular sciences · 2024Article
- Association Between Metabolic Syndrome Inflammatory Biomarkers and COVID-19 Severity.Journal of the Endocrine Society · 2023Article
- Airway Smooth Muscles Contractions in Metabolic Syndrome.Bulletin of experimental biology and medicine · 2022Article
- Therapeutic ketosis decreases methacholine hyperresponsiveness in mouse models of inherent obese asthma.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Linggan Wuwei Jiangxin formula ameliorates airway hyperresponsiveness through suppression of IL-1β and IL-17A expression in allergic asthmatic mice especially with diet-induced obesity.Annals of translational medicine · 2021Article
- Contribution of systemic and airway immune responses to pediatric obesity-related asthma.Paediatric respiratory reviews · 2021Review
- Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation.Journal of clinical medicine · 2021Review
- IL-33, diet-induced obesity, and pulmonary responses to ozone.Respiratory research · 2020Article
- Early life microbiome perturbation alters pulmonary responses to ozone in male mice.Physiological reports · 2020Article
- Androgens augment pulmonary responses to ozone in mice.Physiological reports · 2019Article
- History of Asthma From Childhood and Arterial Stiffness in Asymptomatic Young Adults: The Bogalusa Heart Study.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Augmented Responses to Ozone in Obese Mice Require IL-17A and Gastrin-Releasing Peptide.American journal of respiratory cell and molecular biology · 2018Article
- Obesity promotes prolonged ovalbumin-induced airway inflammation modulating T helper type 1 (Th1), Th2 and Th17 immune responses in BALB/c mice.Clinical and experimental immunology · 2017Article
- Role of ROCK2 in CD4Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017Article
- Mechanisms of Asthma in Obesity. Pleiotropic Aspects of Obesity Produce Distinct Asthma Phenotypes.American journal of respiratory cell and molecular biology · 2016Review
- Obesity, Asthma, and the Microbiome.Physiology (Bethesda, Md.) · 2016Review
- Innate and ozone-induced airway hyperresponsiveness in obese mice: role of TNF-α.American journal of physiology. Lung cellular and molecular physiology · 2015Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Obese mice exhibit innate airway hyperresponsiveness (AHR), a feature of asthma. Tumor necrosis factor alpha (TNFα) is implicated in the disease progression and chronic inflammatory status of both obesity and asthma. TNF acts via two TNF receptors, TNFR1 and TNFR2. To examine the role of TNFR2 in the AHR observed in obese mice, we generated obese Cpe(fat) mice that were either sufficient or deficient in TNFR2 (Cpe(fat) and Cpe(fat)/TNFR2(-/-) mice, respectively) and compared them with their lean controls (WT and TNFR2(-/-) mice). Compared to WT mice, Cpe(fat) mice exhibited AHR to aerosolized methacholine (measured using the forced oscillation technique) which was ablated in Cpe(fat)/TNFR2(-/-) mice. Bioplex or ELISA assay indicated significant increases in serum leptin, G-CSF, IL-7, IL-17A, TNFα, and KC in obese versus lean mice, as well as significant obesity-related increases in bronchoalveolar lavage fluid (BALF) G-CSF and IP-10, regardless of TNFR2 status. Importantly, BALF IL-17A was significantly increased over lean controls in Cpe(fat) but not Cpe(fat)/TNFR2(-/-) mice. Functional annotation clustering of significantly affected genes identified from microarray analysis comparing gene expression in lungs of Cpe(fat) and WT mice, identified blood vessel morphogenesis as the gene ontology category most affected by obesity. This category included several genes associated with AHR, including endothelin and trkB. Obesity increased pulmonary mRNA expression of endothelin and trkB in TNFR2 sufficient but not deficient mice. Our results indicate that TNFR2 signaling is required for the innate AHR that develops in obese mice, and suggest that TNFR2 may act by promoting IL-17A, endothelin, and/or trkB expression.
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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.