ArticleMucosal immunology2019
Colitis susceptibility in mice with reactive oxygen species deficiency is mediated by mucus barrier and immune defense defects.
Article in Mucosal immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 67 citations in OpenAlex.
- The type 1 and type 3 immune responses underlying the tissue inflammation associated with NOX2 deficiency.Frontiers in immunology · 2026Review
- ComparingGut microbes · 2025Article
- Inflammatory targeted nanoplatform incorporated with antioxidative nano iron oxide to attenuate ulcerative colitis progression.iScience · 2025Article
- De novo DUOX2 expression in neutrophil subsets shapes the pathogenesis of intestinal disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Immunometabolism and mitochondria in inflammatory bowel disease: a role for therapeutic intervention?Disease models & mechanisms · 2024Review
- Targeted delivery of Fc-fused PD-L1 for effective management of acute and chronic colitis.Nature communications · 2024Article
- Inflammatory Complications in Chronic Granulomatous Disease.Journal of clinical medicine · 2024Review
- Moxibustion Regulates the BRG1/Nrf2/HO-1 Pathway by Inhibiting MicroRNA-222-3p to Prevent Oxidative Stress in Intestinal Epithelial Cells in Ulcerative Colitis and Colitis-Associated Colorectal Cancer.Journal of immunology research · 2024Article
- The Association between NADPH Oxidase 2 (NOX2) and Drug Resistance in Cancer.Current cancer drug targets · 2024Review
- Article
- Tamarind Seed Polysaccharide Hydrolysate Ameliorates Dextran Sulfate Sodium-Induced Ulcerative Colitis via Regulating the Gut Microbiota.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Article
- Impaired immune response and barrier function in GSPD-1-deficientCurrent research in microbial sciences · 2023Article
- Impact of IBD-Associated Dysbiosis on Bacterial Quorum Sensing Mediated by Acyl-Homoserine Lactone in Human Gut Microbiota.International journal of molecular sciences · 2022Article
- Redox and Metabolic Regulation of Intestinal Barrier Function and Associated Disorders.International journal of molecular sciences · 2022Review
- Germline Variants ofCancers · 2022Article
- New insights into bacterial mechanisms and potential intestinal epithelial cell therapeutic targets of inflammatory bowel disease.Frontiers in microbiology · 2022Review
- Bioluminescence-Based Complementation Assay to Correlate Conformational Changes in Membrane-Bound Complexes with Enzymatic Function.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Bile acids-gut microbiota crosstalk contributes to the improvement of type 2 diabetes mellitus.Frontiers in pharmacology · 2022Review
- Gut microbiota from green tea polyphenol-dosed mice improves intestinal epithelial homeostasis and ameliorates experimental colitis.Microbiome · 2021Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
Reactive oxygen species (ROS) generated by NADPH oxidases (NOX/DUOX) provide antimicrobial defense, redox signaling, and gut barrier maintenance. Inactivating NOX variants are associated with comorbid intestinal inflammation in chronic granulomatous disease (CGD; NOX2) and pediatric inflammatory bowel disease (IBD; NOX1); however Nox-deficient mice do not reflect human disease susceptibility. Here we assessed if a hypomorphic patient-relevant CGD mutation will increase the risk for intestinal inflammation in mice. Cyba (p22
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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.