ArticleMucosal immunology2017
Genetic deletion of the bacterial sensor NOD2 improves murine Crohn's disease-like ileitis independent of functional dysbiosis.
Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Early coconut oil exposure suppresses chronic experimental Crohn's disease via myristic acid and enhanced regulatory T cells.Nature communications · 2026Article
- Resolving the field: a role for Nod2 in T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- Evaluating the Adjuvant Therapeutic Effects of Probiotic StrainsAnimals : an open access journal from MDPI · 2025Article
- Article
- Loss of NOD2 in macrophages improves colitis and tumorigenesis in a lysozyme-dependent manner.Frontiers in immunology · 2023Article
- NOD-like receptors mediate homeostatic intestinal epithelial barrier function: promising therapeutic targets for inflammatory bowel disease.Therapeutic advances in gastroenterology · 2023Review
- Genotype-protein phenotype characterization ofFrontiers in medicine · 2022Article
- NOD-like receptors in autoimmune diseases.Acta pharmacologica Sinica · 2021Review
- NOD2 drives early IL-33-dependent expansion of group 2 innate lymphoid cells during Crohn's disease-like ileitis.The Journal of clinical investigation · 2021Article
- Single-cell atlas of colonic CD8Nature medicine · 2020Article
- NOD1 and NOD2 in inflammatory and infectious diseases.Immunological reviews · 2020Review
- Functional dynamics of bacterial species in the mouse gut microbiome revealed by metagenomic and metatranscriptomic analyses.PloS one · 2020Article
- Innate immune receptors for cross-presentation: The expanding role of NLRs.Molecular immunology · 2019Review
- NOD2 and TLR2 Signal via TBK1 and PI31 to Direct Cross-Presentation and CD8 T Cell Responses.Frontiers in immunology · 2019Article
- Nod2 Deficiency Augments Th17 Responses and Exacerbates Autoimmune Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- The Artificial Sweetener Splenda Promotes Gut Proteobacteria, Dysbiosis, and Myeloperoxidase Reactivity in Crohn's Disease-Like Ileitis.Inflammatory bowel diseases · 2018Article
- 'Cyclical Bias' in Microbiome Research Revealed by A Portable Germ-Free Housing System Using Nested Isolation.Scientific reports · 2018Article
- Emerging Mechanisms of Innate Immunity and Their Translational Potential in Inflammatory Bowel Disease.Frontiers in medicine · 2018Review
- Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn's Disease-Like Ileitis: What is the Right Model?Cellular and molecular gastroenterology and hepatology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Although genetic polymorphisms in NOD2 (nucleotide-binding oligomerization domain-containing 2) have been associated with the pathogenesis of Crohn's disease (CD), little is known regarding the role of wild-type (WT) NOD2 in the gut. To date, most murine studies addressing the role of WT Nod2 have been conducted using healthy (ileitis/colitis-free) mouse strains. Here, we evaluated the effects of Nod2 deletion in a murine model of spontaneous ileitis, i.e., the SAMP1Yit/Fc (SAMP) strain, which closely resembles CD. Remarkably, Nod2 deletion improved both chronic cobblestone ileitis (by 50% assessed, as the % of abnormal mucosa at 24 wks of age), as well as acute dextran sodium sulfate (DSS) colitis. Mechanistically, Th2 cytokine production and Th2-transcription factor activation (i.e., STAT6 phosphorylation) were reduced. Microbiologically, the effects of Nod2 deletion appeared independent of fecal microbiota composition and function, assessed by 16S rRNA and metatranscriptomics. Our findings indicate that pharmacological blockade of NOD2 signaling in humans could improve health in Th2-driven chronic intestinal inflammation.
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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.