NIH RePORTER
Cure8 regulatory brief
Why This Matters
If intestinal stem cells retain an inflammatory “memory,” that could help explain why some people with IBD have persistent barrier problems and repeated flares despite therapy. Discovering durable molecular changes in ISCs might point to new ways to predict healing and to develop treatments that improve mucosal repair.
Who Should Pay Attention
Researchers studying epithelial biology, immune–epithelial interactions, and biomarkers; clinicians interested in mechanisms of mucosal healing in IBD; patients and caregivers interested in research on drivers of relapse and recovery.
Study Snapshot
Story typeRegulatory
Evidence typeFunded research project
Study statusFunded
Source depthResearch project record
What To Know
This is an NIH-funded research project from Mayo Clinic investigating “inflammatory memory” in human intestinal stem cells (ISCs) from patients with IBD.
The team will use patient-derived intestinal organoids from matched inflamed and uninflamed tissue and advanced chromatin profiling and functional assays to study whether prior inflammation leaves durable, chromatin-based imprints on ISCs that alter repair and response to subsequent injury.
The proposal aims to (1) define the molecular mechanisms by which inflammatory memory is encoded, maintained, and recalled in ISCs, and (2) determine how such memory affects epithelial function and susceptibility in IBD.
The investigators plan translational patient stratification studies to explore whether stem cell memory could become a predictive biomarker or therapeutic target for epithelial healing.
This description summarizes the project abstract provided on the NIH Reporter record; it is a project-record summary rather than a peer-reviewed study report and does not present results.
Keep In Mind
This is a funded research project record (NIH Reporter) describing planned work and aims, not a completed study or published results. Findings, timelines, and clinical applications are not reported here. The project uses organoids and chromatin profiling, which are laboratory-based techniques that will require further validation before changing clinical care.
Source Details
Review the original publication for the complete reporting, methods, and context.
Funded research project
Evidence type derived from source or registry metadata.
PublicationNIH RePORTER
AuthorsBrooke R Druliner
InstitutionMAYO CLINIC ROCHESTER
Study typeFunded Research Project
Indexed viaNIH RePORTER
Source typeFunded research record
PublishedSep 4, 2026, 12:00 AM
Content availableResearch project record
Funding disclosed by the source: National Institute of Diabetes and Digestive and Kidney Diseases - R01DK148623 - $688,220
This Cure8 brief is based on source text from the linked article. Cure8 is informational only and is not a substitute for professional medical advice, diagnosis, or treatment.
Dietary-dependent barrier protection by L. rhamnosus GG
This NIH-funded project identifies probiotic metabolic pathways that protect gut barrier integrity in a diet-dependent way, which could explain mixed clinical trial results and point to biomarkers to select patients...
Characterization of uniquely-positioned IL-33-responsive mucosal cells in colitis-associated cancer.
People with longstanding ulcerative colitis face higher colorectal cancer risk; this project focuses on a specific immune/stromal cell population (ST2+ cells responding to IL-33) that may help explain how chronic...
INTERROGATING GCPII-MEDIATED GLUTAMATE SIGNALING IN THE GASTROINTESTINAL TRACT AND ITS ROLE IN INTESTINAL HOMEOSTASIS
This project studies a novel enzyme target (GCPII) that is reportedly upregulated in IBD and may change glutamate signaling and barrier function; understanding it could point to new treatment strategies for people whose...