ArticleThe Journal of experimental medicine2006
The primary defect in experimental ileitis originates from a nonhematopoietic source.
Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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The trial behind it
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Who cites it
90 citing papers in PubMed, 172 citations in OpenAlex.
- Epithelial and stromal remodeling in murine Crohn's disease-like ileitis.bioRxiv : the preprint server for biology · 2025Article
- Dysregulation of γδ intraepithelial lymphocytes precedes Crohn's disease-like ileitis.Science immunology · 2025Article
- Early subclinical stages of the inflammatory bowel diseases: insights from human and animal studies.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- Sex Differences in Colonic Inflammation are Driven by Epithelial-Specific Expression of Estrogen Receptor Alpha.Gastro hep advances · 2025Article
- The epithelium takes the stage in asthma and inflammatory bowel diseases.Frontiers in cell and developmental biology · 2024Review
- Potential Dietary and Therapeutic Strategies Involving Indole-3-Carbinole in Preclinical Models of Intestinal Inflammation.Nutrients · 2023Article
- The yin and yang of B cells in a constant state of battle: intestinal inflammation and inflammatory bowel disease.Frontiers in immunology · 2023Review
- Impact of Epithelial Cell Shedding on Intestinal Homeostasis.International journal of molecular sciences · 2022Review
- Micronutrient Improvement of Epithelial Barrier Function in Various Disease States: A Case for Adjuvant Therapy.International journal of molecular sciences · 2022Review
- Harnessing murine models of Crohn's disease ileitis to advance concepts of pathophysiology and treatment.Mucosal immunology · 2022Review
- Exploring the Early Phase of Crohn's Disease.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2021Review
- E-cadherin activating antibodies limit barrier dysfunction and inflammation in mouse inflammatory bowel disease.Tissue barriers · 2021Article
- Tumor Necrosis Factor's Pathway in Crohn's Disease: Potential for Intervention.International journal of molecular sciences · 2021Review
- T cell protein tyrosine phosphatase protects intestinal barrier function by restricting epithelial tight junction remodeling.The Journal of clinical investigation · 2021Article
- JAK-STAT Pathway Regulation of Intestinal Permeability: Pathogenic Roles and Therapeutic Opportunities in Inflammatory Bowel Disease.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The Gut-Liver Axis in Cholestatic Liver Diseases.Nutrients · 2021Review
- The JAK Inhibitor Tofacitinib Rescues Intestinal Barrier Defects Caused by Disrupted Epithelial-macrophage Interactions.Journal of Crohn's & colitis · 2021Article
- Functional Assessment of Intestinal Permeability and Neutrophil Transepithelial Migration in Mice using a Standardized Intestinal Loop Model.Journal of visualized experiments : JoVE · 2021Article
- Intestinal Stem Cell Niche Defects Result in Impaired 3D Organoid Formation in Mouse Models of Crohn's Disease-like Ileitis.Stem cell reports · 2020Article
- Targeting the Dopaminergic System in Autoimmunity.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
The initiating etiologic factor in Crohn's disease (CD) remains unclear. SAMP1/YitFc (SAMP) mice develop chronic ileitis similar to human CD. We used bone marrow chimeras to determine if SAMP ileitis results from a primary immunological defect or from dysregulated mucosal immunity secondary to intrinsic, nonhematopoietic (e.g., epithelial) dysfunction. SAMP mice receiving wild-type (AKR) BM developed severe ileitis, whereas SAMP BM did not confer ileitis to WT recipients. WT lymphocytes from reconstituted SAMP mice resembled native SAMP populations in regard to surface phenotype and cytokine production. Ilea from native SAMP mice and SAMP recipients of wild-type BM displayed decreased epithelial barrier resistance ex vivo and increased epithelial permeability in vivo compared to native WT mice and AKR recipients of SAMP BM. This permeability defect preceded the development of ileal inflammation, was present in the absence of commensal bacteria, and was accompanied by altered ileal mRNA expression of the tight junction proteins claudin-2 and occludin. Our results provide evidence that the primary defect conferring ileitis in SAMP mice originates from a nonhematopoietic source. Generation of pathogenic lymphocytes is a consequence of this defect and does not reflect intrinsic proinflammatory leukocyte properties. Decreased barrier function suggests that defects in the epithelium may represent the primary source of SAMP ileitis susceptibility.
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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.