ArticleInhalation toxicology2011
Impact of aging on pulmonary responses to acute ozone exposure in mice: role of TNFR1.
Article in Inhalation toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Inconsequential role for chemerin-like receptor 1 in the manifestation of ozone-induced lung pathophysiology in male mice.Physiological reports · 2024Article
- Article
- Augmented Responses to Ozone in Obese Mice Require IL-17A and Gastrin-Releasing Peptide.American journal of respiratory cell and molecular biology · 2018Article
- Article
- Inflammasome, IL-1 and inflammation in ozone-induced lung injury.American journal of clinical and experimental immunology · 2016Review
- 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
- Induction of IL-17A Precedes Development of Airway Hyperresponsiveness during Diet-Induced Obesity and Correlates with Complement Factor D.Frontiers in immunology · 2014Article
- Obesity and airway responsiveness: role of TNFR2.Pulmonary pharmacology & therapeutics · 2013Article
- Augmented pulmonary responses to acute ozone exposure in obese mice: roles of TNFR2 and IL-13.Environmental health perspectives · 2013Article
- Article
- Role of TNFR1 in the innate airway hyperresponsiveness of obese mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
contextChamber studies in adult humans indicate reduced responses to acute ozone with increasing age. Age-related changes in TNFα have been observed. TNFα induced inflammation is predominantly mediated through TNFR1.
objectiveTo examine the impact of aging on inflammatory responses to acute ozone exposure in mice and determine the role of TNFR1 in age-related differences. MATERIALS AND
methodsWildtype and TNFR1 deficient (TNFR1(-/-)) mice aged 7 or 39 weeks were exposed to ozone (2 ppm for 3 h). Four hours after exposure, bronchoalveolar lavage (BAL) was performed and BAL cells, cytokines, chemokines, and protein were examined.
resultsOzone-induced increases in BAL neutrophils and in neutrophil chemotactic factors were lower in 39- versus 7-week-old wildtype, but not (TNFR1(-/-)) mice. There was no effect of TNFR1 genotype in 7-week-old mice, but in 39-week-old mice, BAL neutrophils and BAL concentrations of MCP-1, KC, MIP-2, IL-6 and IP-10 were significantly greater following ozone exposure in TNFR1(-/-) versus wildtype mice. BAL concentrations of the soluble form of the TNFR1 receptor (sTNFR1) were substantially increased in 39-week-old versus 7-week-old mice, regardless of exposure. DISCUSSION AND
conclusionThe data suggest that increased levels of sTNFR1 in the lungs of the 39-week-old mice may neutralize TNFα and protect these older mice against ozone-induced inflammation.
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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.