ArticleToxicology and applied pharmacology2011
Role of TNFR1 in lung injury and altered lung function induced by the model sulfur mustard vesicant, 2-chloroethyl ethyl sulfide.
Article in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Chloropicrin induced ocular injury: Biomarkers, potential mechanisms, and treatments.Toxicology letters · 2024Review
- Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.Disaster medicine and public health preparedness · 2023Review
- Melatonin as Modulator for Sulfur and Nitrogen Mustard-Induced Inflammation, Oxidative Stress and DNA Damage: Molecular Therapeutics.Antioxidants (Basel, Switzerland) · 2023Review
- Pulmonary injury and oxidative stress in rats induced by inhaled sulfur mustard is ameliorated by anti-tumor necrosis factor-α antibody.Toxicology and applied pharmacology · 2021Article
- Assessment of mustard vesicant lung injury and anti-TNF-α efficacy in rodents using live-animal imaging.Annals of the New York Academy of Sciences · 2020Article
- Long-term Respiratory Effects of Mustard Vesicants.Toxicology letters · 2020Review
- Anti-TNFα therapy in inflammatory lung diseases.Pharmacology & therapeutics · 2017Review
- Mustard vesicant-induced lung injury: Advances in therapy.Toxicology and applied pharmacology · 2016Review
- Macrophages and inflammatory mediators in pulmonary injury induced by mustard vesicants.Annals of the New York Academy of Sciences · 2016Review
- Inflammatory mechanisms of pulmonary injury induced by mustards.Toxicology letters · 2016Review
- Attenuation of Nitrogen Mustard-Induced Pulmonary Injury and Fibrosis by Anti-Tumor Necrosis Factor-α Antibody.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation.Experimental and molecular pathology · 2014Article
- Ozone-induced injury and oxidative stress in bronchiolar epithelium are associated with altered pulmonary mechanics.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- Attenuation of acute nitrogen mustard-induced lung injury, inflammation and fibrogenesis by a nitric oxide synthase inhibitor.Toxicology and applied pharmacology · 2012Article
- Prolonged injury and altered lung function after ozone inhalation in mice with chronic lung inflammation.American journal of respiratory cell and molecular biology · 2012Article
- Role of reactive nitrogen species generated via inducible nitric oxide synthase in vesicant-induced lung injury, inflammation and altered lung functioning.Toxicology and applied pharmacology · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Lung toxicity induced by sulfur mustard is associated with inflammation and oxidative stress. To elucidate mechanisms mediating pulmonary damage, we used 2-chloroethyl ethyl sulfide (CEES), a model sulfur mustard vesicant. Male mice (B6129) were treated intratracheally with CEES (3 or 6 mg/kg) or control. Animals were sacrificed 3, 7 or 14 days later and bronchoalveolar lavage (BAL) fluid and lung tissue collected. Treatment of mice with CEES resulted in an increase in BAL protein, an indication of alveolar epithelial damage, within 3 days. Expression of Ym1, an oxidative stress marker also increased in the lung, along with inducible nitric oxide synthase, and at 14 days, cyclooxygenase-2 and monocyte chemotactic protein-1, inflammatory proteins implicated in tissue injury. These responses were attenuated in mice lacking the p55 receptor for TNFα (TNFR1-/-), demonstrating that signaling via TNFR1 is key to CEES-induced injury, oxidative stress, and inflammation. CEES-induced upregulation of CuZn-superoxide dismutase (SOD) and MnSOD was delayed or absent in TNFR1-/- mice, relative to WT mice, suggesting that TNFα mediates early antioxidant responses to lung toxicants. Treatment of WT mice with CEES also resulted in functional alterations in the lung including decreases in compliance and increases in elastance. Additionally, methacholine-induced alterations in total lung resistance and central airway resistance were dampened by CEES. Loss of TNFR1 resulted in blunted functional responses to CEES. These effects were most notable in the airways. These data suggest that targeting TNFα signaling may be useful in mitigating lung injury, inflammation and functional alterations induced by vesicants.
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