Cure8 research brief
This funded NIH project investigates how EAEC and AIEC bacteria might drive intestinal inflammation by degrading MUC3A/MUC4 and disrupting receptor tyrosine kinase signaling—mechanisms that could underlie infection-associated colitis and contribute to IBD risk.
Researchers in mucosal immunology and microbiome–host interactions; clinicians interested in infection-related triggers of IBD; patients and advocates tracking basic research into IBD causes.
This NIH-funded project uses human intestinal organoids (colonoids) to study how enteric bacteria—specifically Enteroaggregative E. coli (EAEC) and Adherent‑Invasive E. coli (AIEC)—may trigger intestinal inflammation by degrading transmembrane mucins MUC3A and MUC4.
The team will test whether bacterial C2S-family proteases disrupt receptor tyrosine kinase signaling and goblet cell function, and will analyze affected cell-signaling pathways at single‑cell resolution.
The work focuses on two aims: (1) defining how C2S protease–mediated cleavage of MUC3/4 alters tyrosine kinase stability and downstream signaling at the single-cell level in human colonoids, and (2) determining how MUC3/4 degradation by EAEC and AIEC affects innate immunity, inflammation, and mucosal barrier function to inform potential interventions.
This is a project-record summary of planned and ongoing laboratory research using human intestinal organoids; it does not report completed clinical results. Interpretations and any translational applications will depend on future experimental findings.
Review the original publication for the complete reporting, methods, and context.
Funding disclosed by the source: National Institute of Allergy and Infectious Diseases - R21AI202149 - $253,445
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.
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