ArticleApoptosis : an international journal on programmed cell death2016
Eosinophil resistance to glucocorticoid-induced apoptosis is mediated by the transcription factor NFIL3.
Article in Apoptosis : an international journal on programmed cell death, 2016. 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, 45 citations in OpenAlex.
- Mechanisms of glucocorticoid resistance in hypereosinophilic syndromes.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Trial
- Rediscovering eosinophil identity through tissue adaptation.Nature immunology · 2026Review
- Identification of Prognostic Values of Neutrophil Extracellular Traps-Related Genes in Glioma Based on Bioinformatics.Immunity, inflammation and disease · 2026Article
- Accumulation of long-chain unsaturated fatty acids in the airway inflammatory microenvironment drives eosinophil etosis and corticosteroid resistance.Cell communication and signaling : CCS · 2025Article
- Macrophage membrane coated nanoscale coordination polymers promote graft survival in allogeneic transplantation.Journal of nanobiotechnology · 2025Article
- Defining the Blood Cytokine Profile in Asthma to Understand Asthma Heterogeneity.Immunity, inflammation and disease · 2025Article
- PIM1 signaling in immunoinflammatory diseases: an emerging therapeutic target.Frontiers in immunology · 2024Review
- The role of mitochondria in eosinophil function: implications for severe asthma pathogenesis.Frontiers in cell and developmental biology · 2024Review
- Article
- Higher Body Mass Index Is Associated With Decreased Treatment Response to Topical Steroids in Eosinophilic Esophagitis.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2023Article
- Gene-Smoking Interaction Analysis for the Identification of Novel Asthma-Associated Genetic Factors.International journal of molecular sciences · 2023Article
- Inadequate therapeutic responses to glucocorticoid treatment in bronchial asthma.The Journal of international medical research · 2023Review
- NFIL3 and its immunoregulatory role in rheumatoid arthritis patients.Frontiers in immunology · 2022Article
- Recent advances of eosinophils and its correlated diseases.Frontiers in public health · 2022Review
- Marine-Derived Compounds for the Potential Treatment of Glucocorticoid Resistance in Severe Asthma.Marine drugs · 2021Review
- Hypereosinophilic syndrome with multiorgan involvement: an interdisciplinary work-up.BMJ case reports · 2021Article
- Apoptosis of Eosinophil Granulocytes.Biology · 2020Review
- Activation of Group 2 Innate Lymphoid Cells via TL1A/DR3. A Solution to Corticosteroid Resistance?American journal of respiratory and critical care medicine · 2020Article
- Nuclear Receptors in Asthma: Empowering Classical Molecules Against a Contemporary Ailment.Frontiers in immunology · 2020Review
- Senescence in Pulmonary Fibrosis: Between Aging and Exposure.Frontiers in medicine · 2020Review
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
The mainstay of asthma therapy, glucocorticoids (GCs) exert their therapeutic effects through the inhibition of inflammatory signaling and induction of eosinophil apoptosis. However, laboratory and clinical observations of GC-resistant asthma suggest that GCs' effects on eosinophil viability may depend on the state of eosinophil activation. In the present study we demonstrate that eosinophils stimulated with IL-5 show impaired pro-apoptotic response to GCs. We sought to determine the contribution of GC-mediated transactivating (TA) and transrepressing (TR) pathways in modulation of activated eosinophils' response to GC by comparing their response to the selective GC receptor (GR) agonist Compound A (CpdA) devoid of TA activity to that upon treatment with Dexamethasone (Dex). IL-5-activated eosinophils showed contrasting responses to CpdA and Dex, as IL-5-treated eosinophils showed no increase in apoptosis compared to cells treated with Dex alone, while CpdA elicited an apoptotic response regardless of IL-5 stimulation. Proteomic analysis revealed that both Nuclear Factor IL-3 (NFIL3) and Map Kinase Phosphatase 1 (MKP1) were inducible by IL-5 and enhanced by Dex; however, CpdA had no effect on NFIL3 and MKP1 expression. We found that inhibiting NFIL3 with specific siRNA or by blocking the IL-5-inducible Pim-1 kinase abrogated the protective effect of IL-5 on Dex-induced apoptosis, indicating crosstalk between IL-5 anti-apoptotic pathways and GR-mediated TA signaling occurring via the NFIL3 molecule. Collectively, these results indicate that (1) GCs' TA pathway may support eosinophil viability in IL-5-stimulated cells through synergistic upregulation of NFIL3; and (2) functional inhibition of IL-5 signaling (anti-Pim1) or the use of selective GR agonists that don't upregulate NFIL3 may be effective strategies for the restoring pro-apoptotic effect of GCs on IL-5-activated eosinophils.
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