ArticleInternational immunopharmacology2012
Inhalation of sulfur mustard causes long-term T cell-dependent inflammation: possible role of Th17 cells in chronic lung pathology.
Article in International immunopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 49 citations in OpenAlex.
- Vitamin D3 and deconvoluting a rash.JCI insight · 2023Trial
- Circular RNA circSmad4 controls pulmonary fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.Disaster medicine and public health preparedness · 2023Review
- The role of PD-1/PD-L1 axis in idiopathic pulmonary fibrosis: Friend or foe?Frontiers in immunology · 2022Review
- Mast Cells Promote Nitrogen Mustard-Mediated Toxicity in the Lung Associated With Proinflammatory Cytokine and Bioactive Lipid Mediator Production.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- 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
- Pulmonary toxicants and fibrosis: innate and adaptive immune mechanisms.Toxicology and applied pharmacology · 2020Review
- Long-term Respiratory Effects of Mustard Vesicants.Toxicology letters · 2020Review
- Polydatin ameliorates pulmonary fibrosis by suppressing inflammation and the epithelial mesenchymal transitionRSC advances · 2019Article
- The systemic nature of mustard lung: Comparison with COPD patients.Interdisciplinary toxicology · 2017Review
- Mustard vesicant-induced lung injury: Advances in therapy.Toxicology and applied pharmacology · 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
- Characterization of Lung Fibroblasts More than Two Decades after Mustard Gas Exposure.PloS one · 2015Article
- The injury progression of T lymphocytes in a mouse model with subcutaneous injection of a high dose of sulfur mustard.Military Medical Research · 2014Article
- Pathway reconstruction of airway remodeling in chronic lung diseases: a systems biology approach.PloS one · 2014Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Sulfur mustard (SM) is a highly toxic chemical warfare agent that remains a threat to human health. The immediate symptoms of pulmonary distress may develop into chronic lung injury characterized by progressive lung fibrosis, the major cause of morbidity among the surviving SM victims. Although SM has been intensely investigated, little is known about the mechanism(s) by which SM induces chronic lung pathology. Increasing evidence suggests that IL-17(+) cells are critical in fibrosis, including lung fibrotic diseases. In this study we exposed F344 rats and cynomolgus monkeys to SM via inhalation and determined the molecular and cellular milieu in their lungs at various times after SM exposure. In rats, SM induced a burst of pro-inflammatory cytokines/chemokines within 72 h, including IL-1β, TNF-α, IL-2, IL-6, CCL2, CCL3, CCL11, and CXCL1 that was associated with neutrophilic infiltration into the lung. At 2 wks and beyond (chronic phase), lymphocytic infiltration and continued elevated expression of cytokines/chemokines were sustained. TGF-β, which was undetectable in the acute phase, was strongly upregulated in the chronic phase; these conditions persisted until the animals were sacrificed. The chronic phase was also associated with myofibroblast proliferation, collagen deposition, and presence of IL-17(+) cells. At ≥30 days, SM inhalation promoted the accumulation of IL-17(+) cells in the inflamed areas of monkey lungs. Thus, SM inhalation causes acute and chronic inflammatory responses; the latter is characterized by the presence of TGF-β, fibrosis, and IL-17(+) cells in the lung. IL-17(+) cells likely play an important role in the pathogenesis of SM-induced lung injury.
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