ArticleToxicological sciences : an official journal of the Society of Toxicology2019
Regulation of Macrophage Foam Cell Formation During Nitrogen Mustard (NM)-Induced Pulmonary Fibrosis by Lung Lipids.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Potential association of bronchoalveolar lavage lipid-laden macrophages with disease severity and corticosteroid response in interstitial lung disease: a pilot study.Journal of thoracic disease · 2026Article
- Altered cholesterol immunometabolism activates the macrophage NLRP3-inflammasome in lung fibrosis.American journal of respiratory cell and molecular biology · 2026Article
- Targeting immunosenescence in lung diseases: mechanistic insights and clinical interventions.BMC medicine · 2026Review
- Comprehensive reexamination of the acute toxicity of nitrogen mustards: HN-1, HN-2 and HN-3 as blister agents: application of multi in silico approach.Archives of toxicology · 2025Article
- Shared pathogenic mechanisms linking obesity and idiopathic pulmonary fibrosis revealed by bioinformatics and in vivo validation.Scientific reports · 2025Article
- Unravelling the Programmed Inflammation and Tissue Repair by a Multipotential Antimicrobial K21 Silane.International dental journal · 2025Article
- Farnesoid X receptor (FXR) as a potential therapeutic target for lung diseases: a narrative review.Journal of thoracic disease · 2024Review
- Progesterone amplifies allergic inflammation and airway pathology in association with higher lung ILC2 responses.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Lipid-Laden Macrophages in Pulmonary Diseases.Cells · 2024Review
- Toxicological inhalation studies in rats to substantiate grouping of zinc oxide nanoforms.Particle and fibre toxicology · 2024Article
- The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases.Lipids in health and disease · 2024Review
- Suppression of Lung Oxidative Stress, Inflammation, and Fibrosis following Nitrogen Mustard Exposure by the Selective Farnesoid X Receptor Agonist Obeticholic Acid.The Journal of pharmacology and experimental therapeutics · 2024Article
- Spatial and phenotypic heterogeneity of resident and monocyte-derived macrophages during inflammatory exacerbations leading to pulmonary fibrosis.Frontiers in immunology · 2024Article
- CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.Respiratory research · 2023Article
- Overlapping Science in Radiation and Sulfur Mustard Exposures of Skin and Lung: Consideration of Models, Mechanisms, Organ Systems, and Medical Countermeasures: Overlapping science in radiation and sulfur mustard injuries to lung and skin.Disaster medicine and public health preparedness · 2023Article
- Etiology of lipid-laden macrophages in the lung.International immunopharmacology · 2023Review
- Steady-state estradiol triggers a unique innate immune response to allergen resulting in increased airway resistance.Biology of sex differences · 2023Article
- Farnesoid X receptor regulates lung macrophage activation and injury following nitrogen mustard exposure.Toxicology and applied pharmacology · 2022Article
- Intratracheal Administration of Acyl Coenzyme A Acyltransferase-1 Inhibitor K-604 Reduces Pulmonary Inflammation Following Bleomycin-Induced Lung Injury.The Journal of pharmacology and experimental therapeutics · 2022Article
- MG53 attenuates nitrogen mustard-induced acute lung injury.Journal of cellular and molecular medicine · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Nitrogen mustard (NM) is a vesicant known to target the lung, causing acute injury which progresses to fibrosis. Evidence suggests that activated macrophages contribute to the pathologic response to NM. In these studies, we analyzed the role of lung lipids generated following NM exposure on macrophage activation and phenotype. Treatment of rats with NM (0.125 mg/kg, i.t.) resulted in a time-related increase in enlarged vacuolated macrophages in the lung. At 28 days postexposure, macrophages stained positively for Oil Red O, a marker of neutral lipids. This was correlated with an accumulation of oxidized phospholipids in lung macrophages and epithelial cells and increases in bronchoalveolar lavage fluid (BAL) phospholipids and cholesterol. RNA-sequencing and immunohistochemical analysis revealed that lipid handling pathways under the control of the transcription factors liver-X receptor (LXR), farnesoid-X receptor (FXR), peroxisome proliferator-activated receptor (PPAR)-ɣ, and sterol regulatory element-binding protein (SREBP) were significantly altered following NM exposure. Whereas at 1-3 days post NM, FXR and the downstream oxidized low-density lipoprotein receptor, Cd36, were increased, Lxr and the lipid efflux transporters, Abca1 and Abcg1, were reduced. Treatment of naïve lung macrophages with phospholipid and cholesterol enriched large aggregate fractions of BAL prepared 3 days after NM exposure resulted in upregulation of Nos2 and Ptgs2, markers of proinflammatory activation, whereas large aggregate fractions prepared 28 days post NM upregulated expression of the anti-inflammatory markers, Il10, Cd163, and Cx3cr1, and induced the formation of lipid-laden foamy macrophages. These data suggest that NM-induced alterations in lipid handling and metabolism drive macrophage foam cell formation, potentially contributing to the development of pulmonary fibrosis.
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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.