ArticleNature communications2015
Glucocorticoids suppress inflammation via the upregulation of negative regulator IRAK-M.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 2 of them syntheses that pooled it.
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Who cites it
77 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.
- Pooled it
- Pooled it
- Glucocorticoid-Induced Proteome and Phosphoproteome Changes in Breast Cancer Cell Lines.Journal of proteome research · 2026Article
- Article
- IRAK signaling in cancers: mechanisms, targeting, and clinical implications.Expert opinion on investigational drugs · 2025Review
- Differential RELA and GR recruitment to the BIRC3/BIRC2 locus: Molecular insight as to combinatorial regulation by proinflammatory cytokines and glucocorticoid.Molecular pharmacology · 2025Article
- The Impact of Stress on Autoimmune Disorders: Type 1 Diabetes Mellitus and Systemic Lupus Erythematosus.Cureus · 2025Review
- Integrated analysis of bioinformatics, mendelian randomization, and experimental validation reveals novel diagnostic and therapeutic targets for osteoarthritis: progesterone as a potential therapeutic agent.Journal of orthopaedic surgery and research · 2025Article
- Defining the Differential Corticosteroid Response Basis from Multiple Omics Approaches.International journal of molecular sciences · 2024Review
- Glucocorticoid therapy for acute respiratory distress syndrome: Current concepts.Journal of intensive medicine · 2024Review
- Adaptor molecules mediate negative regulation of macrophage inflammatory pathways: a closer look.Frontiers in immunology · 2024Review
- Ecdysteroids from the Korean Endemic SpeciesACS omega · 2023Article
- Increased expression of miR146a dysregulates TLR2-induced HBD2 in airway epithelial cells from patients with COPD.ERJ open research · 2023Article
- IRAK-M has effects in regulation of lung epithelial inflammation.Respiratory research · 2023Article
- IRAK-M Regulates Proliferative and Invasive Phenotypes of Lung Fibroblasts.Inflammation · 2023Article
- Glucocorticoids and medroxyprogesterone acetate synergize with inflammatory stimuli to selectively upregulate CCL20 transcription.Molecular and cellular endocrinology · 2023Article
- Identification of immune-associated genes in diagnosing osteoarthritis with metabolic syndrome by integrated bioinformatics analysis and machine learning.Frontiers in immunology · 2023Article
- Regulation of innate immune signaling by IRAK proteins.Frontiers in immunology · 2023Review
- Phase-separation: a possible new layer for transcriptional regulation by glucocorticoid receptor.Frontiers in endocrinology · 2023Review
- Negative Cross-Talk between TLR2/4-Independent AMPKα1 and TLR2/4-Dependent JNK RegulatesJournal of immunology (Baltimore, Md. : 1950) · 2022Article
17 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
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Glucocorticoids are among the most commonly used anti-inflammatory agents. Despite the enormous efforts in elucidating the glucocorticoid-mediated anti-inflammatory actions, how glucocorticoids tightly control overactive inflammatory response is not fully understood. Here we show that glucocorticoids suppress bacteria-induced inflammation by enhancing IRAK-M, a central negative regulator of Toll-like receptor signalling. The ability of glucocorticoids to suppress pulmonary inflammation induced by non-typeable Haemophilus influenzae is significantly attenuated in IRAK-M-deficient mice. Glucocorticoids improve the survival rate after a lethal non-typeable Haemophilus influenzae infection in wild-type mice, but not in IRAK-M-deficient mice. Moreover, we show that glucocorticoids and non-typeable Haemophilus influenzae synergistically upregulate IRAK-M expression via mutually and synergistically enhancing p65 and glucocorticoid receptor binding to the IRAK-M promoter. Together, our studies unveil a mechanism by which glucocorticoids tightly control the inflammatory response and host defense via the induction of IRAK-M and may lead to further development of anti-inflammatory therapeutic strategies.
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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.