ArticleImmunology2020
Histone hyperacetylation mediates enhanced IL-1β production in LPS/IFN-γ-stimulated macrophages.
Article in Immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- Targeting the sirtuin 6-NF-κB p65 axis by 6-hydroxyhyoscyamine hydrobromide: a deacetylation-driven new therapy for diabetic wounds.Cellular & molecular biology letters · 2026Article
- SCFAs' pleiotropic role in pathogenesis and salutogenesis: mechanisms in exacerbation and regulation of inflammation and fibrosis from gut to host.Journal of medical microbiology · 2026Review
- The impact of dyslipidemia on skeletal health - from an immunoregulatory perspective.Frontiers in immunology · 2026Review
- Diverse RNA methylation patterns in neutrophils: key drivers in hepatocellular carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Bioinformatics Approach to Identifying Molecular Targets of Isoliquiritigenin Affecting Chronic Obstructive Pulmonary Disease: A Machine Learning Pharmacology Study.International journal of molecular sciences · 2025Article
- Histone modifications and metabolic reprogramming in tumor-associated macrophages: a potential target of tumor immunotherapy.Frontiers in immunology · 2025Review
- Multi-omics and multi-stages integration identified a novel variant associated with silicosis risk.Archives of toxicology · 2024Article
- A Narrative Review: Immunometabolic Interactions of Host-Gut Microbiota and Botanical Active Ingredients in Gastrointestinal Cancers.International journal of molecular sciences · 2024Review
- Berberine promotes M2 macrophage polarisation through the IL-4-STAT6 signalling pathway in ulcerative colitis treatment.Heliyon · 2023Article
- Sirtuin-dependent metabolic and epigenetic regulation of macrophages during tuberculosis.Frontiers in immunology · 2023Review
- The Role of Myeloid Cells in GBM Immunosuppression.Frontiers in immunology · 2022Review
- Deficiency of Myeloid Pfkfb3 Protects Mice From Lung Edema and Cardiac Dysfunction in LPS-Induced Endotoxemia.Frontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Under the condition of lipopolysaccharide (LPS)/interferon (IFN)-γ activation, macrophage metabolism is converted from oxidative phosphorylation to glycolysis. In the present work, we analysed whether glycolysis could affect interleukin (IL)-1β expression through altering histone acetylation levels in mouse bone marrow-derived macrophages. Immunocytochemistry and Western blot analysis are used to characterize histone acetylation in macrophages stimulated by LPS/IFN-γ. Real-time polymerase chain reaction and enzyme-linked immunosorbent assay were used to determine IL-1β production. The metabolism of macrophages was monitored in real-time by the Seahorse test. Our results showed that glycolytic metabolism could enhance histone acetylation and promote IL-1β production in LPS/IFN-γ-activated macrophages. Moreover, increased production of IL-1β by glycolysis was mediated through enhanced H3K9 acetylation. Importantly, it was found that a high dose of histone deacetylase inhibitor could also significantly increase the expression of IL-1β in the absence of glycolytic metabolism. In conclusion, this study demonstrates that glycolytic metabolism could regulate IL-1β expression by increasing histone acetylation levels in LPS/IFN-γ-stimulated macrophages.
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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.