ArticleGut2025
DUOX2 activation drives bacterial translocation and subclinical inflammation in IBD-associated dysbiosis.
Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Lactobacillus johnsonii BS15 Alleviates Fluoride-Induced Intestinal Barrier Injury by Regulating the RhoA/ROCK-Mediated Cytoskeletal Remodeling.Probiotics and antimicrobial proteins · 2026Article
- Toll-like receptor 2 impacts small intestinal villus capillarization through epithelial dual oxidase 2.Redox biology · 2026Article
- Malondialdehyde Drives a Feed-Forward Reactive Oxygen Species Loop in Pediatric Crohn's Disease.Digestive diseases and sciences · 2026Article
- Enzyme-Responsive Polymeric Drug Delivery Systems for the Treatment of Inflammatory Bowel Diseases: A Review.Polymers · 2026Review
- DUOX2-Driven Oxidative Stress Alters the Gut Redox Niche and Promotes Microbial Dysbiosis in Crohn's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Extracellular Redox Balance as a Determinant of Immune Regulation and Tissue Inflammation.Antioxidants (Basel, Switzerland) · 2026Review
- [Verbenalin ameliorates intestinal inflammation and colitis in a mouse model of Crohn's disease by inhibiting the PI3K-AKT pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Uncovering a novel treatment strategy: sodium butyrate overcomes cisplatin resistance in the oral squamous cell carcinoma by inducing ferroptosis.Journal of experimental & clinical cancer research : CR · 2026Article
- Integrated multi-omics analysis reveals distinct microbiota-metabolite signatures and a novel HCN2-2-hydroxybutyric acid interaction in inflammatory bowel disease.Frontiers in nutrition · 2026Article
- Microbial metabolic memory in inflammatory bowel disease: microbiota-derived metabolites, host-microbe reprogramming, and relapse susceptibility.Frontiers in microbiology · 2026Review
- Generative AI-augmented transcriptomic and microbiome analysis across inflammatory and fibrotic disease states in Crohn's disease.Frontiers in artificial intelligence · 2026Article
- FMT and Bifidobacterium quadruple viable tablets supplementation modulate gut microbiota to ameliorate high-altitude exposure induced colonic injury.Frontiers in microbiology · 2026Article
- Selenium: A Key Element in Inflammatory Bowel Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Elevated DUOX2 levels correlate with necrotizing enterocolitis development.Frontiers in cellular and infection microbiology · 2025Article
- Salivary oxidative stress persists in inflammatory bowel disease regardless of biological treatment response.Frontiers in pharmacology · 2025Article
- Recent advancements and comprehensive analyses of butyric acid in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
backgroundInflammatory bowel diseases (IBDs) are characterised by dysbiosis and a leaky gut. The NADPH oxidase dual oxidase 2 (DUOX2) is upregulated in patients with IBD, yet its role in driving the disease remains unclear.
objectiveWe interrogated the functional consequences of epithelial DUOX2 activity for the host and microbiome.
designDUOX2 function was studied in mice with epithelial-specific DUOX2 overactivation (vTLR4), inactivation (vTLR4 DUOXA IEC-KO) and wild-type controls. We assessed the effect of dysbiosis on DUOX2 signalling and intestinal permeability (FITC-dextran, serum zonulin, bacterial translocation) with germ-free (GF) mice engrafted with IBD or healthy microbiota. RNA sequencing of colonic mucosa and microbiota and faecal metabolomics were used to characterise the host-microbe interface. Mechanistic studies were conducted in mouse colonoids, IBD biopsies and patient serum samples.
resultsDUOX2 activity increased permeability and bacterial translocation and induced subclinical inflammation in vTLR4 mice. GF vTLR4 mice had increased DUOX2 activity and permeability but no subclinical inflammation. In patients with IBD, DUOX2 expression was positively associated with plasma zonulin levels and negatively associated with ZO-1 expression. Engraftment of GF mice with IBD stool increased DUOX2 activity and triggered low-grade inflammation and permeability defects in mice. DUOX2 activity functionally altered the microbiome, reduced butyrate metabolism and promoted proinflammatory and pro-oncogenic bacterial metabolites. Butyrate and histone deacetylase (HDAC) inhibitors blocked DUOX2 activation and reversed its effects.
conclusionsElevated DUOX2 signalling contributes to epithelial barrier dysfunction, microbiome alterations and subclinical inflammation. Butyrate and HDAC inhibitors reversed these effects, indicating that DUOX2 may be a therapeutic target in IBD.
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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.