ArticleFrontiers in immunology2018
The IL-33 Receptor ST2 Regulates Pulmonary Inflammation and Fibrosis to Bleomycin.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Parasite-Derived IL-33 Inhibitors Prevent Bleomycin-Induced Lung Fibrosis.European journal of immunology · 2026Article
- Blocking interleukin 33 reduces joint, systemic, and lung inflammatory responses in the combined collagen-induced arthritis-inhalant endotoxin exposure model.The Journal of pharmacology and experimental therapeutics · 2026Article
- The predictive value of combined detection of serum IL-33, TSLP and eosinophils in the treatment effect and exacerbation risk of chronic obstructive pulmonary disease.BMC pulmonary medicine · 2026Article
- Activation of TSLP-IL-9 Axis Hinders the Antifibrotic Effect of ST2 Deficiency in Pulmonary Fibrosis.International journal of molecular sciences · 2025Article
- Targeting JNK1/2 and P38 Mitogen-Activated Protein Kinases With Pazopanib Mitigates Bleomycin-Induced Lung Fibrosis.Archiv der Pharmazie · 2025Article
- IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
- 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
- Review
- 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
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- Role of the IL-33/ST2 Activation Pathway in the Development of the Hepatic Fibrosis Induced byInternational journal of molecular sciences · 2023Article
- The IL-33:ST2 axis is unlikely to play a central fibrogenic role in idiopathic pulmonary fibrosis.Respiratory research · 2023Article
- Immune Mechanisms of Pulmonary Fibrosis with Bleomycin.International journal of molecular sciences · 2023Review
- A comparative study of IL-33 and its receptor ST2 in a C57BL/6 J mouse model of pulmonary Cryptococcus neoformans infection.Medical microbiology and immunology · 2023Article
- Plasma Cytokine Profiling Reveals Differences between Silicotic Patients with Simple Silicosis and Those with Progressive Massive Fibrosis Caused by Engineered Stone.International journal of molecular sciences · 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
- Coal dust exposure triggers heterogeneity of transcriptional profiles in mouse pneumoconiosis and Vitamin D remedies.Particle and fibre toxicology · 2022Article
- Role of nuclear factor-kappa B in bleomycin induced pulmonary fibrosis and the probable alleviating role of ginsenoside: histological, immunohistochemical, and biochemical study.Anatomy & cell biology · 2021Article
- Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis is a progressive, devastating, and yet untreatable fibrotic disease of unknown origin. Interleukin-33 (IL-33), an IL-1 family member acts as an alarmin with pro-inflammatory properties when released after stress or cell death. Here, we investigated the role of IL-33 in the bleomycin (BLM)-induced inflammation and fibrosis model using mice IL-33 receptor [chain suppression of tumorigenicity 2 (ST2)] mice compared with C57BL/6 wild-type mice. Unexpectedly, 24 h post-BLM treatment ST2-deficient mice displayed augmented inflammatory cell recruitment, in particular by neutrophils, together with enhanced levels of chemokines and remodeling factors in the bronchoalveolar space and/or the lungs. At 11 days, lung remodeling and fibrosis were decreased with reduced M2 macrophages in the lung associated with M2-like cytokine profile in ST2-deficient mice, while lung cellular inflammation was decreased but with fluid retention (edema) increased.
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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.