ArticleAmerican journal of respiratory cell and molecular biology2016
Characterization of Distinct Macrophage Subpopulations during Nitrogen Mustard-Induced Lung Injury and Fibrosis.
Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 88 citations in OpenAlex.
- Vitamin D3 and deconvoluting a rash.JCI insight · 2023Trial
- The interplay between vitamin D3 and Nrf2 signaling: mechanistic insights and therapeutic potentials.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- IL-9R/Arg1 pathway promotes polyamine metabolism in human airway macrophages.The Journal of allergy and clinical immunology · 2026Article
- Molecular Determinants of Macrophage Polarization in Glioblastoma and Implications for Tumor Progression.Cells · 2026Article
- Cannabinoid-2 Receptor Activation Attenuates Sulfur Mustard Analog 2-Chloroethyl-Ethyl-Sulfide-Induced Acute Lung Injury in Mice.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Reactive Oxygen Species in Asthma: Regulators of Macrophage Polarization and Therapeutic Implications: A Narrative Review.Journal of asthma and allergy · 2025Review
- Immunometabolic programming of macrophages in asthma pathogenesis and therapy.Frontiers in physiology · 2025Review
- Identification of early events in nitrogen mustard pulmonary toxicity that are independent of infiltrating inflammatory cells using precision cut lung slices.Toxicology and applied pharmacology · 2024Article
- Role of macrophage bioenergetics in N-acetylcysteine-mediated mitigation of lung injury and oxidative stress induced by nitrogen mustard.Toxicology and applied pharmacology · 2024Article
- 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
- Epigenetic mechanisms of alveolar macrophage activation in chemical-induced acute lung injury.Frontiers in immunology · 2024Review
- Spatial and phenotypic heterogeneity of resident and monocyte-derived macrophages during inflammatory exacerbations leading to pulmonary fibrosis.Frontiers in immunology · 2024Article
- APC and ZBTB2 May Mediate M2 Macrophage Infiltration to Promote the Development of Renal Fibrosis: A Bioinformatics Analysis.BioMed research international · 2024Article
- 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
- Targeting Tumor Necrosis Factor Alpha to Mitigate Lung Injury Induced by Mustard Vesicants and Radiation.Disaster medicine and public health preparedness · 2023Review
- Article
- Chemical exposure and alveolar macrophages responses: 'the role of pulmonary defense mechanism in inhalation injuries'.BMJ open respiratory research · 2023Review
- Pulmonary Fibrosis Related to Amiodarone-Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review.Diagnostics (Basel, Switzerland) · 2022Review
- Doxycycline hyclate stimulates inducible nitric oxide synthase and arginase imbalance, potentiating inflammatory and oxidative lung damage in schistosomiasis.Biomedical journal · 2022Article
- Farnesoid X receptor regulates lung macrophage activation and injury following nitrogen mustard exposure.Toxicology and applied pharmacology · 2022Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Nitrogen mustard (NM) is an alkylating agent known to cause extensive pulmonary injury progressing to fibrosis. This is accompanied by a persistent macrophage inflammatory response. In these studies, we characterized the phenotype of macrophages accumulating in the lung over time following NM exposure. Treatment of rats with NM (0.125 mg/kg, intratracheally) resulted in an increase in CD11b(+) macrophages in histologic sections. These cells consisted of inducible nitric oxide synthase(+) (iNOS) proinflammatory M1 macrophages, and CD68(+), CD163(+), CD206(+), YM-1(+), and arginase-II(+)antiinflammatory M2 macrophages. Although M1 macrophages were prominent 1-3 days after NM, M2 macrophages were most notable at 28 days. At this time, they were enlarged and vacuolated, consistent with a profibrotic phenotype. Flow cytometric analysis of isolated lung macrophages identified three phenotypically distinct subpopulations: mature CD11b(-), CD43(-), and CD68(+) resident macrophages, which decreased in numbers after NM; and two infiltrating (CD11b(+)) macrophage subsets: immature CD43(+) M1 macrophages and mature CD43(-) M2 macrophages, which increased sequentially. Time-related increases in M1 (iNOS, IL-12α, COX-2, TNF-α, matrix metalloproteinase-9, matrix metalloproteinase-10) and M2 (IL-10, pentraxin-2, connective tissue growth factor, ApoE) genes, as well as chemokines/chemokine receptors associated with trafficking of M1 (CCR2, CCR5, CCL2, CCL5) and M2 (CX3CR1, fractalkine) macrophages to sites of injury, were also noted in macrophages isolated from the lung after NM. The appearance of M1 and M2 macrophages in the lung correlated with NM-induced acute injury and the development of fibrosis, suggesting a potential role of these macrophage subpopulations in the pathogenic response to NM.
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