ArticleJournal of immunology (Baltimore, Md. : 1950)2015
IRAK-M promotes alternative macrophage activation and fibroproliferation in bleomycin-induced lung injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 72 citations in OpenAlex.
- Cadherin-11 integrates Piezo1 and interleukin-6 signaling to promote fibroblast activation.Biomaterials science · 2026Article
- Identification and Validation of Liver Transplantation-Induced Acute Lung Injury Biomarkers Using a Bioinformatics and Experimental Approach.Annals of transplantation · 2026Article
- Cadherin-11 integrates Piezo1 and interleukin-6 signaling to promote fibroblast activation.bioRxiv : the preprint server for biology · 2025Article
- M2 macrophage co-culture overrides viscoelastic hydrogel mechanics to promote IL6-dependent fibroblast activation.Cell biomaterials · 2025Article
- IRAK3 is upregulated in rheumatoid arthritis synovium and delays the onset of experimental arthritis.Frontiers in immunology · 2025Article
- Direct M2 macrophage co-culture overrides viscoelastic hydrogel mechanics to promote fibroblast activation.bioRxiv : the preprint server for biology · 2024Article
- Immunomodulation of Macrophages in Diabetic Wound Individuals by Structurally Diverse Bioactive Phytochemicals.Pharmaceuticals (Basel, Switzerland) · 2024Review
- NFATc3 Promotes Pulmonary Inflammation and Fibrosis by Regulating Production of CCL2 and CXCL2 in Macrophages.Aging and disease · 2023Article
- IRAK-M has effects in regulation of lung epithelial inflammation.Respiratory research · 2023Article
- IRAK-M Regulates Proliferative and Invasive Phenotypes of Lung Fibroblasts.Inflammation · 2023Article
- Salt-inducible kinase 2 regulates fibrosis during bleomycin-induced lung injury.The Journal of biological chemistry · 2022Article
- Plasticity towards Rigidity: A Macrophage Conundrum in Pulmonary Fibrosis.International journal of molecular sciences · 2022Review
- Lung Pneumonitis and Fibrosis in Cancer Therapy: A Review on Cellular and Molecular Mechanisms.Current drug targets · 2022Review
- Pooled CRISPR screening identifies mScience advances · 2021Article
- IRAK-M knockout promotes allergic airway inflammation, but not airway hyperresponsiveness, in house dust mite-induced experimental asthma model.Journal of thoracic disease · 2021Article
- IRAK-M Regulates Monocyte Trafficking to the Lungs in Response to Bleomycin Challenge.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Macrophage HIF-1α mediates obesity-related adipose tissue dysfunction via interleukin-1 receptor-associated kinase M.American journal of physiology. Endocrinology and metabolism · 2020Article
- PAI-1 Regulation of TGF-β1-induced Alveolar Type II Cell Senescence, SASP Secretion, and SASP-mediated Activation of Alveolar Macrophages.American journal of respiratory cell and molecular biology · 2020Article
- Generation of bone marrow chimeras using X-ray irradiation: comparison to cesium irradiation and use in immunotherapy.Journal of biological methods · 2020Article
- Schisandra Inhibit Bleomycin-Induced Idiopathic Pulmonary Fibrosis in Rats via Suppressing M2 Macrophage Polarization.BioMed research international · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis is a devastating lung disease characterized by inflammation and the development of excessive extracellular matrix deposition. Currently, there are only limited therapeutic intervenes to offer patients diagnosed with pulmonary fibrosis. Although previous studies focused on structural cells in promoting fibrosis, our study assessed the contribution of macrophages. Recently, TLR signaling has been identified as a regulator of pulmonary fibrosis. IL-1R-associated kinase-M (IRAK-M), a MyD88-dependent inhibitor of TLR signaling, suppresses deleterious inflammation, but may paradoxically promote fibrogenesis. Mice deficient in IRAK-M (IRAK-M(-/-)) were protected against bleomycin-induced fibrosis and displayed diminished collagen deposition in association with reduced production of IL-13 compared with wild-type (WT) control mice. Bone marrow chimera experiments indicated that IRAK-M expression by bone marrow-derived cells, rather than structural cells, promoted fibrosis. After bleomycin, WT macrophages displayed an alternatively activated phenotype, whereas IRAK-M(-/-) macrophages displayed higher expression of classically activated macrophage markers. Using an in vitro coculture system, macrophages isolated from in vivo bleomycin-challenged WT, but not IRAK-M(-/-), mice promoted increased collagen and α-smooth muscle actin expression from lung fibroblasts in an IL-13-dependent fashion. Finally, IRAK-M expression is upregulated in peripheral blood cells from idiopathic pulmonary fibrosis patients and correlated with markers of alternative macrophage activation. These data indicate expression of IRAK-M skews lung macrophages toward an alternatively activated profibrotic phenotype, which promotes collagen production, leading to the progression of experimental 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.