ArticleRespiratory research2008
IFN-gamma, IL-4 and IL-13 modulate responsiveness of human airway smooth muscle cells to IL-13.
Article in Respiratory research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Asthma susceptible genes in Chinese population: a meta-analysis.Respiratory research · 2010Pooled it
- Leptin augments IL-13-induced airway eotaxins and submucosal eosinophilia in obesity-associated asthma.The Journal of allergy and clinical immunology · 2025Article
- Determining the toxicological effects of indoor air pollution on both a healthy and an inflammatory-comprised model of the alveolar epithelial barrier in vitro.Particle and fibre toxicology · 2024Article
- Epithelial-Mesenchymal Transition Mechanisms in Chronic Airway Diseases: A Common Process to Target?International journal of molecular sciences · 2023Review
- New insights into the pathophysiology and therapeutic targets of asthma and comorbid chronic rhinosinusitis with or without nasal polyposis.Clinical science (London, England : 1979) · 2023Review
- Airway remodeling heterogeneity in asthma and its relationship to disease outcomes.Frontiers in physiology · 2023Review
- Cavin-1 promotes M2 macrophages/microglia polarization via SOCS3.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Repeated exposure of house dust mite induces progressive airway inflammation in mice: Differential roles of CCL17 and IL-13.Pharmacology research & perspectives · 2021Article
- The Clusters of Transcription Factors NFATC2, STAT5, GATA2, AP1, RUNX1 and EGR2 Binding Sites at the InducedJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Intranasal instillation of miR‑410 targeting IL‑4/IL‑13 attenuates airway inflammation in OVA‑induced asthmatic mice.Molecular medicine reports · 2019Article
- Crosstalk Between Signaling Pathways Involved in the Regulation of Airway Smooth Muscle Cell Hyperplasia.Frontiers in pharmacology · 2019Review
- Th2 Cytokines Augment IL-31/IL-31RA Interactions via STAT6-dependent IL-31RA Expression.The Journal of biological chemistry · 2015Article
- Human parainfluenza virus type 3 (HPIV3) induces production of IFNγ and RANTES in human nasal epithelial cells (HNECs).Journal of inflammation (London, England) · 2015Article
- A molecular perspective on TH2-promoting cytokine receptors in patients with allergic disease.The Journal of allergy and clinical immunology · 2014Review
- Dissociation of FK506-binding protein 12.6 kD from ryanodine receptor in bronchial smooth muscle cells in airway hyperresponsiveness in asthma.American journal of respiratory cell and molecular biology · 2014Article
- IL-13 R110Q, a Naturally Occurring IL-13 Polymorphism, Confers Enhanced Functional Activity in Cultured Human Bronchial Smooth Muscle Cells.Allergy, asthma & immunology research · 2013Article
- Airway smooth muscle in the pathophysiology and treatment of asthma.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Review
- MAPK regulation of IL-4/IL-13 receptors contributes to the synergistic increase in CCL11/eotaxin-1 in response to TGF-β1 and IL-13 in human airway fibroblasts.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Aqueous extracts from dietary supplements influence the production of inflammatory cytokines in immortalized and primary T lymphocytes.BMC complementary and alternative medicine · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIL-13 is a critical mediator of allergic asthma and associated airway hyperresponsiveness. IL-13 acts through a receptor complex comprised of IL-13Ralpha1 and IL-4Ralpha subunits with subsequent activation of signal transducer and activator of transcription 6 (STAT6). The IL-13Ralpha2 receptor may act as a decoy receptor. In human airway smooth muscle (HASM) cells, IL-13 enhances cellular proliferation, calcium responses to agonists and induces eotaxin production. We investigated the effects of pre-treatment with IL-4, IL-13 and IFN-gamma on the responses of HASM cells to IL-13.
methodsCultured HASM were examined for expression of IL-13 receptor subunits using polymerase chain reaction, immunofluorescence microscopy and flow cytometry. Effects of cytokine pre-treatment on IL-13-induced cell responses were assessed by looking at STAT6 phosphorylation using Western blot, eotaxin secretion and calcium responses to histamine.
resultsIL-13Ralpha1, IL-4Ralpha and IL-13Ralpha2 subunits were expressed on HASM cells. IL-13 induced phosphorylation of STAT6 which reached a maximum by 30 minutes. Pre-treatment with IL-4, IL-13 and, to a lesser degree, IFN-gamma reduced peak STAT6 phosphorylation in response to IL-13. IL-13, but not IFN-gamma, pre-treatment abrogated IL-13-induced eotaxin secretion. Pre-treatment with IL-4 or IL-13 abrogated IL-13-induced augmentation of the calcium transient evoked by histamine. Cytokine pre-treatment did not affect expression of IL-13Ralpha1 and IL-4Ralpha but increased expression of IL-13Ralpha2. An anti-IL-13Ralpha2 neutralizing antibody did not prevent the cytokine pre-treatment effects on STAT6 phosphorylation. Cytokine pre-treatment increased SOCS-1, but not SOCS-3, mRNA expression which was not associated with significant increases in protein expression.
conclusionPre-treatment with IL-4 and IL-13, but not IFN-gamma, induced desensitization of the HASM cells to IL-13 as measured by eotaxin secretion and calcium transients to histamine. The mechanism of IL-4 and IL-13 induced desensitization does not appear to involve either downregulation of receptor expression or induction of the IL-13Ralpha2 or the SOCS proteins.
Indexed as
Identifiers
What OpenQuestion holds
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.