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Updated: May 7, 2026

Important Endpoints and Proliferative Markers to Assess Small Intestinal Injury and Adaptation using a Mouse Model of Chemotherapy-Induced Mucositis
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MICROBIOME AND INFLAMMASOME ALTERATIONS FOUND DURING RADIATION DOSE FINDING IN A SINCLAIR MINIPIG MODEL OF

Timothy S Horseman, Babita Parajuli1, Andrew M Frank2

  • 1Armed Forces Radiobiology Research Institute, Uniformed Services University of the Health Sciences, Bethesda, Maryland.

Shock (Augusta, Ga.)
|July 16, 2024
PubMed
Summary
This summary is machine-generated.

This study establishes the Sinclair minipig as a model for gastrointestinal acute radiation syndrome (GI-ARS), demonstrating dose-dependent symptoms and mortality. Findings reveal radiation-induced gut barrier damage and microbial shifts, offering therapeutic targets for radiation exposure.

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Area of Science:

  • Radiation biology
  • Gastroenterology
  • Microbiology

Background:

  • Abdominal radiotherapy and nuclear events can cause gastrointestinal acute radiation syndrome (GI-ARS).
  • GI-ARS compromises intestinal barrier integrity, increasing infection risk.
  • Physiologically relevant animal models are essential for studying GI-ARS and identifying therapeutic targets.

Purpose of the Study:

  • To establish radiation dose requirements for inducing GI-ARS in Sinclair minipigs.
  • To characterize the clinical, pathological, and microbiological changes associated with GI-ARS in this model.
  • To identify potential therapeutic and diagnostic targets for radiation exposure.

Main Methods:

  • Sinclair minipigs were exposed to lower hemibody radiation doses of 8, 10, or 12 Gy.
  • Animals were monitored for GI-ARS symptoms, weight loss, diarrhea, and mortality over 14 days.
  • Necropsy included histological analysis, western blotting for inflammatory markers (NLRP3, IL-1β), serum citrulline measurement, and gut microbiota analysis.

Main Results:

  • A dose-dependent increase in weight loss, diarrhea severity, and mortality was observed.
  • Radiation significantly reduced villi length and decreased serum citrulline, indicating intestinal damage.
  • Increased bacterial translocation, NLRP3 and IL-1β levels, and significant gut microbial community shifts were noted post-irradiation.

Conclusions:

  • The Sinclair minipig model effectively replicates dose-dependent GI-ARS clinical symptoms.
  • Radiation exposure induces intestinal barrier dysfunction, inflammation, and alterations in gut microbiota.
  • This model provides insights into GI-ARS pathophysiology and identifies potential targets for interventions after radiation exposure.