ArticleThe Journal of clinical investigation1993
Regulation of alveolar macrophage transforming growth factor-beta secretion by corticosteroids in bleomycin-induced pulmonary inflammation in the rat.
Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 185 citations in OpenAlex.
- Adjuvant interferon gamma in patients with drug - resistant pulmonary tuberculosis: a pilot study.BMC infectious diseases · 2004Trial
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- Glycolysis and beyond in glucose metabolism: exploring pulmonary fibrosis at the metabolic crossroads.Frontiers in endocrinology · 2024Review
- Differential early response of monocyte/macrophage subsets to intra-operative corticosteroid administration in lung transplantation.Frontiers in immunology · 2023Article
- An Agent-Based Model of Radiation-Induced Lung Fibrosis.International journal of molecular sciences · 2022Article
- Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.The Japanese dental science review · 2022Review
- The Restoring Effect of Human Umbilical Cord-Derived Mesenchymal Cell-Conditioned Medium (hMSC-CM) against Carbon Tetrachloride-Induced Pulmonary Fibrosis in Male Wistar Rats.International journal of inflammation · 2022Article
- Recent Insights into Cellular Crosstalk in Respiratory and Gastrointestinal Mucosal Immune Systems.Immune network · 2020Review
- Glucocorticoids Shape Macrophage Phenotype for Tissue Repair.Frontiers in immunology · 2019Review
- IL23 and TGF-ß diminish macrophage associated metastasis in pancreatic carcinoma.Scientific reports · 2018Article
- Transforming growth factor-β in stem cells and tissue homeostasis.Bone research · 2018Article
- Bax-inhibiting peptide attenuates bleomycin-induced lung injury in mice.Biology open · 2017Article
- AQX-1125, small molecule SHIP1 activator inhibits bleomycin-induced pulmonary fibrosis.British journal of pharmacology · 2017Article
- MicroRNA-27a-3p Is a Negative Regulator of Lung Fibrosis by Targeting Myofibroblast Differentiation.American journal of respiratory cell and molecular biology · 2016Article
- Endocytosis of indium-tin-oxide nanoparticles by macrophages provokes pyroptosis requiring NLRP3-ASC-Caspase1 axis that can be prevented by mesenchymal stem cells.Scientific reports · 2016Article
- Vagotomy attenuates bleomycin-induced pulmonary fibrosis in mice.Scientific reports · 2015Article
- A pneumocyte-macrophage paracrine lipid axis drives the lung toward fibrosis.American journal of respiratory cell and molecular biology · 2015Article
- Estrogen Signaling Modulates Allergic Inflammation and Contributes to Sex Differences in Asthma.Frontiers in immunology · 2015Review
- Current and emerging pharmacological treatments for sarcoidosis: a review.Drug design, development and therapy · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a model of pulmonary inflammation and fibrosis induced by the antineoplastic antibiotic, bleomycin, we previously demonstrated that TGF-beta was markedly elevated within 7 d of bleomycin administration. At the time of maximal TGF-beta production, TGF-beta 1 was localized by immunohistochemistry to be present almost exclusively in alveolar macrophages. In this study, we have demonstrated that alveolar macrophages stimulated by bleomycin-induced injury secrete large quantities of biologically active TGF-beta 1 when explanted into tissue culture. However, alveolar macrophages from normal saline-treated rats secrete small quantities of biologically inactive TGF-beta. In contrast, splenic macrophages secrete large quantities of inactive TGF-beta and are unaffected by the intratracheal bleomycin treatment. High doses of the corticosteroid methylprednisolone given intramuscularly before and concomitantly with bleomycin administration prevented the influx of alveolar macrophages into the lungs, diminishing both the number of macrophages present in the alveoli and the total lung content of TGF-beta. However, the rate of secretion of TGF-beta by alveolar macrophages recovered from the alveoli was unchanged after corticosteroid treatment. When activated alveolar macrophages were cultured in the presence of several concentrations of dexamethasone that completely suppressed IL-1 secretion, little effect on TGF-beta secretion was observed. The findings in this study demonstrate that during bleomycin-induced injury, alveolar macrophages not only secrete large quantities of active TGF-beta 1, but are a predominant source of the enhanced TGF-beta response seen in this model. Furthermore, the alveolar macrophage secretion of TGF-beta is not inhibited by the presence of high concentrations of corticosteroids.
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