ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Protective role of spleen-derived macrophages in lung inflammation, injury, and fibrosis induced by nitrogen mustard.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 42 citations in OpenAlex.
- Vitamin D3 and deconvoluting a rash.JCI insight · 2023Trial
- IL-9R/Arg1 pathway promotes polyamine metabolism in human airway macrophages.The Journal of allergy and clinical immunology · 2026Article
- Prognostic risk model based on cholesterol metabolism-Associated gene module for idiopathic pulmonary fibrosis.PloS one · 2026Article
- Emerging Role of Splenic Macrophage in Malaria Pathogenesis and Immunity.Immunity, inflammation and disease · 2025Review
- Parenchymal and inflammatory responses to ozone exposure in the aging healthy and surfactant protein C mutant lung.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Effects of injury size on local and systemic immune cell dynamics in volumetric muscle loss.NPJ Regenerative medicine · 2025Article
- Review
- Effects of injury size on local and systemic immune cell dynamics in volumetric muscle loss.bioRxiv : the preprint server for biology · 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
- 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
- Topical application of synthetic melanin promotes tissue repair.NPJ Regenerative medicine · 2023Article
- Roles of alpha-7 nicotinic acetylcholine receptors and spleen in the lung injury induced by a repeated saline lavage in rat.BMC pulmonary medicine · 2022Article
- Parenchymal and Inflammatory Cell Responses to Single and Repeated Ozone Exposure in Healthy and Surfactant Protein-C Mutant Lung.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- MG53 attenuates nitrogen mustard-induced acute lung injury.Journal of cellular and molecular medicine · 2022Article
- Comparison of Long-Term Pneumonia Risk between Spleen Injury and Non-Spleen Injury after Total Splenectomy-A Population-Based Study.Journal of personalized medicine · 2022Article
- Immunophenotyping of Acute Inflammatory Exacerbations of Lung Injury Driven by Mutant Surfactant Protein-C: A Role for Inflammatory Eosinophils.Frontiers in pharmacology · 2022Article
- Dietary glucosinolates inhibit splenic inflammation in high fat/cholesterol diet-fed C57BL/6 mice.Nutrition research and practice · 2021Article
- Macrophage activation in the lung during the progression of nitrogen mustard induced injury is associated with histone modifications and altered miRNA expression.Toxicology and applied pharmacology · 2021Article
- Role of Innate Immune System in Environmental Lung Diseases.Current allergy and asthma reports · 2021Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Nitrogen mustard (NM) is a vesicant that causes lung injury and fibrosis, accompanied by a persistent macrophage inflammatory response. In these studies we analyzed the spleen as a source of these cells. Splenectomized (SPX) and sham control rats were treated intratracheally with NM (0.125 mg/kg) or PBS control. Macrophage responses were analyzed 1-7 days later. Splenectomy resulted in an increase in lung macrophages expressing CCR2, but a decrease in ATR-1α(+) cells, receptors important in bone marrow and spleen monocyte trafficking, respectively. Splenectomy was also associated with an increase in proinflammatory M1 (iNOS(+), CD11b(+)CD43(+)) macrophages in lungs of NM-treated rats, as well as greater upregulation of iNOS and COX-2 mRNA expression. Conversely, a decrease in CD11b(+)CD43(-) M2 macrophages was observed in SPX rats, with no changes in CD68(+), CD163(+), CD206(+), or YM-1(+) M2 macrophages, suggesting distinct origins of M2 subpopulations responding to NM. Macrophage expression of M2 genes including IL-10, ApoE, PTX-2, PTX-3, 5-HT2α, and 5-HT7 was also reduced in NM-treated SPX rats compared with shams, indicating impaired M2 activity. Changes in lung macrophages responding to NM as a consequence of splenectomy were correlated with exacerbated tissue injury and more rapid fibrogenesis. These data demonstrate that the spleen is a source of a subset of M2 macrophages with anti-inflammatory activity; moreover, in their absence, proinflammatory/cytotoxic M1 macrophages predominate in the lung, resulting in heightened pathology. Understanding the origin of macrophages and characterizing their phenotype after vesicant exposure may lead to more targeted therapeutics aimed at reducing toxicity and disease pathogenesis.
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