ArticleCellular and molecular gastroenterology and hepatology2024
BRD4 Regulates Glycolysis-Dependent Nos2 Expression in Macrophages Upon H pylori Infection.
Article in Cellular and molecular gastroenterology and hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 20 citations in OpenAlex.
- A single-cell multi-omics atlas defines the cellular and molecular landscape of gastric intestinal metaplasia.Journal of translational medicine · 2026Article
- Review
- Bromodomain-containing protein 4 in inflammatory diseases: molecular mechanisms and therapeutic potential.Journal of inflammation (London, England) · 2026Review
- Research Status and Prospects ofGastroenterology research and practice · 2026Review
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- Glucolipid Metabolic Disorders andInternational journal of endocrinology · 2026Review
- Hub genes and common pathogenic mechanisms between COPD and H. pylori infection.Journal, genetic engineering & biotechnology · 2025Article
- BRD4 regulates PAI-1 expression in tumor-associated macrophages to drive chemoresistance in colorectal cancer.Oncogene · 2025Article
- BRD4 as the key lactylation related gene in heart failure identified through bioinformatics analysis.Scientific reports · 2025Article
- Targeting BRD4 ameliorates experimental emphysema by disrupting super-enhancer in polarized alveolar macrophage.Respiratory research · 2025Article
- Helicobacter pylori infection promotes M1 macrophage polarization and gastric inflammation by activation of NLRP3 inflammasome via TNF/TNFR1 axis.Cell communication and signaling : CCS · 2025Article
- Metabolic reprogramming inFrontiers in cellular and infection microbiology · 2025Review
- Metabolic regulation of the immune system in health and diseases: mechanisms and interventions.Signal transduction and targeted therapy · 2024Review
- Endogenous glucocorticoids are required for normal macrophage activation and gastricAmerican journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Comparison of gastric inflammation and metaplasia induced byMicrobiology spectrum · 2024Article
- Trained Immunity and Trained Tolerance: The Case ofInternational journal of molecular sciences · 2024Review
- Current research on the interaction between Helicobacter pylori and macrophages.Molecular biology reports · 2024Review
- BRD4 Empowers Macrophages to Fight Helicobacter pylori.Cellular and molecular gastroenterology and hepatology · 2024Article
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8 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsMetabolic reprogramming is essential for the activation and functions of macrophages, including bacterial killing and cytokine production. Bromodomain-containing protein 4 (BRD4) has emerged as a critical regulator of innate immune response. However, the potential role of BRD4 in the metabolic reprogramming of macrophage activation upon Helicobacter pylori infection remains unclear.
methodsBone marrow-derived macrophages (BMDMs) from wild-type (WT) and Brd4-myeloid deletion conditional knockout (Brd4-CKO) mice were infected with H pylori. RNA sequencing was performed to evaluate the differential gene expression between WT and Brd4-deficient BMDMs upon infection. An in vivo model of H pylori infection using WT and Brd4-CKO mice was used to confirm the role of BRD4 in innate immune response to infection.
resultsDepletion of Brd4 in BMDMs showed impaired H pylori-induced glycolysis. In addition, H pylori-induced expression of glycolytic genes, including Slc2a1 and Hk2, was decreased in Brd4-deficient BMDMs. BRD4 was recruited to the promoters of Slc2a1 and Hk2 via hypoxia-inducible factor-1α, facilitating their expression. BRD4-mediated glycolysis stabilized H pylori-induced nitric oxide synthase (Nos2) messenger RNA to produce nitric oxide. The NO-mediated killing of H pylori decreased in Brd4-deficient BMDMs, which was rescued by pyruvate. Furthermore, Brd4-CKO mice infected with H pylori showed reduced gastric inflammation and increased H pylori colonization with reduced inducible NO synthase expression in gastric macrophages.
conclusionsOur study identified BRD4 as a key regulator of hypoxia-inducible factor-1α-dependent glycolysis and macrophage activation. Furthermore, we show a novel regulatory role of BRD4 in innate immunity through glycolysis to stabilize Nos2 messenger RNA for NO production to eliminate H pylori infection.
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