ArticleAmerican journal of respiratory cell and molecular biology2013
Interleukin-33 potentiates bleomycin-induced lung injury.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 117 citations in OpenAlex.
- Parasite-Derived IL-33 Inhibitors Prevent Bleomycin-Induced Lung Fibrosis.European journal of immunology · 2026Article
- Collaborative functionality between three types of inflammation in idiopathic pulmonary fibrosis.Nature immunology · 2026Review
- COPD Biologics: Right Patient, Right Pathway, Right Time.Pulmonary therapy · 2026Review
- Beyond inflammation: alarmins as critical drivers of pulmonary fibrosis.ERJ open research · 2026Review
- Activation of TSLP-IL-9 Axis Hinders the Antifibrotic Effect of ST2 Deficiency in Pulmonary Fibrosis.International journal of molecular sciences · 2025Article
- Innovation through imitation: IL-33 decoys show promise in pulmonary fibrosis.The Journal of pharmacology and experimental therapeutics · 2025Article
- Therapeutic targeting of full-length interleukin-33 protein levels with cell-permeable decoy peptides attenuates fibrosis in the bleomycin model in vivo.The Journal of pharmacology and experimental therapeutics · 2025Article
- Choosing the proper animal model for oral submucous fibrosis research: considerations and challenges.Frontiers in physiology · 2025Review
- Revisiting pulmonary fibrosis: inflammatory dynamics of the lipofibroblast-to-inflammatory lipofibroblast-to-activated myofibroblast reversible switch.Frontiers in immunology · 2025Review
- The IL-33/ST2 Axis Is Not Required for the Profibrotic Effect of IL-33 in the Lungs.American journal of respiratory cell and molecular biology · 2024Article
- Serum alarmins and the risk of incident interstitial lung disease in rheumatoid arthritis.Rheumatology (Oxford, England) · 2024Article
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- Enter the Matrix: Fibroblast-immune cell interactions shape extracellular matrix deposition in health and disease.F1000Research · 2024Review
- The modulation of immune cell death in connection to microRNAs and natural products.Frontiers in immunology · 2024Review
- Unpacking the complexity of nuclear IL-33 (nIL-33): a crucial regulator of transcription and signal transduction.Journal of cell communication and signaling · 2023Review
- Allies or enemies? The effect of regulatory T cells and related T lymphocytes on the profibrotic environment in bleomycin-injured lung mouse models.Clinical and experimental medicine · 2023Review
- The IL-33:ST2 axis is unlikely to play a central fibrogenic role in idiopathic pulmonary fibrosis.Respiratory research · 2023Article
- Full-length IL-33 augments pulmonary fibrosis in an ST2- and Th2-independent, non-transcriptomic fashion.Cellular immunology · 2023Article
- The potential role of interleukin (IL)-25/IL-33/thymic stromal lymphopoietin (TSLP) on the pathogenesis of idiopathic pulmonary fibrosis.The clinical respiratory journal · 2022Review
- Ischemia reperfusion injury facilitates lung allograft acceptance through IL-33-mediated activation of donor-derived IL-5 producing group 2 innate lymphoid cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms of interstitial lung disease (ILD) remain incompletely understood, although recent observations have suggested an important contribution by IL-33. Substantial elevations in IL-33 expression were found in the lungs of patients with idiopathic pulmonary fibrosis and scleroderma lung disease, as well as in the bleomycin injury mouse model. Most of the observed IL-33 expression was intracellular and intranuclear, suggesting involvement of the full-length (fl) protein, but not of the proteolytically processed mature IL-33 cytokine. The effects of flIL-33 on mouse lungs were assessed independently and in combination with bleomycin injury, using recombinant adenovirus-mediated gene delivery. Bleomycin-induced changes were not affected by gene deficiency of the IL-33 receptor T1/ST2. Combined flIL-33 expression and bleomycin injury exerted a synergistic effect on pulmonary lymphocyte and collagen accumulation, which could be explained by synergistic regulation of the cytokines transforming growth factor-β, IL-6, monocyte chemotactic protein-1, macrophage inflammatory protein\x{2013}1α, and tumor necrosis factor-α. By contrast, no increase in the levels of the Th2 cytokines IL-4, IL-5, or IL-13 was evident. Moreover, flIL-33 was found to increase the expression of several heat shock proteins (HSPs) significantly, and in particular HSP70, which is known to be associated with ILD. Thus, flIL-33 is a synergistic proinflammatory and profibrotic regulator that acts by stimulating the expression of several non-Th2 cytokines, and activates the expression of HSP70.
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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.