ArticleThe Journal of clinical investigation1994
Steroid-resistant asthma. Cellular mechanisms contributing to inadequate response to glucocorticoid therapy.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
What it found
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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
66 citing papers in PubMed, 395 citations in OpenAlex.
- Trial
- Differential connectivity of gene regulatory networks distinguishes corticosteroid response in asthma.The Journal of allergy and clinical immunology · 2018Trial
- The effects of airway microbiome on corticosteroid responsiveness in asthma.American journal of respiratory and critical care medicine · 2013Trial
- In vitro glucocorticoid sensitivity is associated with clinical glucocorticoid therapy outcome in rheumatoid arthritis.Arthritis research & therapy · 2012Trial
- Vitamin D levels, lung function, and steroid response in adult asthma.American journal of respiratory and critical care medicine · 2010Trial
- Evaluating the Anti-inflammatory Potential of JN-KI3: The Therapeutic Role of PI3Kγ-Selective Inhibitors in Asthma Treatment.Inflammation · 2025Article
- NR3C1 variants and glucocorticoid response in childhood nephrotic syndrome in North India.BMC nephrology · 2025Article
- Novel Perspectives of TSLP and RXR Signaling in Corticosteroid-Resistant Asthma: Updates on TSLP Blockers.Current medicinal chemistry · 2025Review
- circ-0001875 downregulation is associated with M1 macrophage activation and lung inflammation in severe asthma.Frontiers in immunology · 2025Article
- The Glucocorticoid Receptor: Isoforms, Functions, and Contribution to Glucocorticoid Sensitivity.Endocrine reviews · 2024Review
- Glucocorticoid Insensitivity in Asthma: The Unique Role for Airway Smooth Muscle Cells.International journal of molecular sciences · 2022Review
- Assessment of the Link ofJournal of advanced research · 2021Article
- Review
- Blood tryptase and thymic stromal lymphopoietin levels predict the risk of exacerbation in severe asthma.Scientific reports · 2021Observational
- Long non-coding RNA growth arrest specific-5: a potential biomarker for early diagnosis of severe asthma.Journal of thoracic disease · 2020Article
- Unmet needs in asthma.Therapeutics and clinical risk management · 2019Review
- Disease- and treatment-associated acquired glucocorticoid resistance.Endocrine connections · 2018Review
- Steroid resistance of airway type 2 innate lymphoid cells from patients with severe asthma: The role of thymic stromal lymphopoietin.The Journal of allergy and clinical immunology · 2018Article
- Role of IL-15 in the modulation of TGF-β1-mediated inflammation in asthma.Experimental and therapeutic medicine · 2017Article
- 17-oxo-DHA displays additive anti-inflammatory effects with fluticasone propionate and inhibits the NLRP3 inflammasome.Scientific reports · 2016Article
6 more citing papers are in PubMed but not listed here.
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 3 institutions in 1 country.
Funding
Abstract
The current study examined whether alterations in glucocorticoid receptor (GR) binding contribute to poor response to glucocorticoid therapy in asthma. 29 asthma patients with forced expiratory volume in 1 s (FEV1) < 70% predicted were studied. Patients were classified as steroid sensitive (SS) if their morning FEV1 increased > 30% after a 1-wk course of oral prednisone 20 mg twice daily and steroid resistant (SR) if they failed to increase > 15%. PBMC obtained from these two groups, 17 SR and 12 SS, as well as 12 normal controls were analyzed. SR patients had two distinguishable GR binding abnormalities: 15 of the 17 SR patients demonstrated a significantly reduced GR binding affinity, as compared with SS patients (P = 0.0001) and normal controls (P = 0.0001). This defect was localized to T cells and reverted to normal after 48 h in culture media. However, incubation with a combination of IL-2 and IL-4 sustained this abnormality. The other two SR patients had an abnormally low GR number with normal binding affinity that was not limited to T cells. Furthermore, GR number failed to normalize after incubation in media alone or IL-2 and IL-4. Therefore, SR asthma may be due to more than one abnormality, the majority related to a reversible cytokine-induced reduction in GR binding affinity and the second related to an irreversible reduction in GR number. These findings may have important implications for the design of alternative treatment approaches for recalcitrant asthma.
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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.