ArticleAmerican journal of respiratory cell and molecular biology2023
IL-1β Induces a Proinflammatory Fibroblast Microenvironment that Impairs Lung Progenitors' Function.
Article in American journal of respiratory cell and molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 24 citations in OpenAlex.
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- Chemotherapy induces an IL1β-dependent neutrophil recruitment and activation that promote chemoresistance in metastatic ovarian cancer.Journal for immunotherapy of cancer · 2026Article
- IL-1β-mediated interaction between Müller cells and microglia through CXCL1/5-CXCR2 aggravates visual dysfunction in experimental glaucoma.Journal of neuroinflammation · 2026Article
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Dysplastic Epithelial Repair Propagates Chronic Pathology Through the Paracrine Transformation of Pulmonary Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- Functional siRNA Delivery via Jet Nebulization: Proof-of-Concept IL-1ß Silencing in Macrophage-like THP-1 Cells.International journal of molecular sciences · 2026Article
- Pyroptosis, A Double-Edged Sword in Respiratory Diseases: A Narrative Review.Journal of inflammation research · 2026Review
- The role and therapeutic advances of neutrophils in acute myocardial infarction: from traditional chinese medicine modulation to modern therapeutic strategies.Chinese medicine · 2025Review
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- Transcriptomic Comparisons of Somatic and Cancer Stem Cells.Biomedicines · 2025Review
- Recent advances in the role of gasotransmitters in necroptosis.Apoptosis : an international journal on programmed cell death · 2025Review
- Fibroblast-derived osteoglycin promotes epithelial cell repair.NPJ Regenerative medicine · 2025Article
- Lung organoids in COPD: recent advances and future prospects.Respiratory research · 2025Review
- [Prospects of Smoking Hazards Research Using Lung Organoid].Jugan geon-gang gwa jilbyeong · 2025Review
- Neurodegenerative diseases and neuroinflammation-induced apoptosis.Open life sciences · 2025Review
- Bronchial epithelial cell-derived extracellular vesicles drive inflammasome activation andFrontiers in immunology · 2025Article
- Electroacupuncture at Zusanli regulates the pathological phenotype of inflammatory bowel disease by modulating the NLRP3 inflammasome pathway.Immunity, inflammation and disease · 2024Article
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9 authors at 4 institutions in 2 countries.
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Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by a persistent inflammatory state in the lungs and defective tissue repair. Although the inflammatory response in patients with COPD is well characterized and known to be exaggerated during exacerbations, its contribution to lung injury and abnormal repair is still unclear. In this study, we aimed to investigate how the inflammatory microenvironment affects the epithelial progenitors and their supporting mesenchymal niche cells involved in tissue repair of the distal lung. We focused on IL-1β, a key inflammatory mediator that is increased during exacerbations of COPD, and used an organoid model of lung epithelial cells and fibroblasts to assess the effect of IL-1β treatment on these cells' transcriptome and secreted factors. Whereas direct treatment of the lung organoids with IL-1β promoted organoid growth, this switched toward inhibition when it was added as fibroblast pretreatment followed by organoid treatment. We then investigated the IL-1β-driven mechanisms in the fibroblasts and found an inflammatory response related to (C-X-C motif) ligand (CXCL) chemokines; we confirmed that these chemokines were responsible for the impaired organoid growth and found that targeting their C-X-C chemokine receptors 1/2 (CXCR1/2) receptors or the IL-1β intracellular signaling reduced the proinflammatory response and restored organoid growth. These data demonstrate that IL-1β alters the fibroblasts' state by promoting a distinct inflammatory response, switching their supportive function on epithelial progenitors toward an inhibitory one in an organoid assay. These results imply that chronic inflammation functions as a shift toward inhibition of repair, thereby contributing to chronic inflammatory diseases like COPD.
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