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Updated: Jul 17, 2026

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291
Published on: December 10, 2016
Ileal mucosal response to bacterial toxin challenge
Y Harari1, N W Weisbrodt, F G Moody
1Department of Surgery, University of Texas-Houston Health Science Center, 77225, USA.
The bacterial toxin formyl-methionyl leucyl phenylalanine (FMLP) may initiate intestinal barrier disruption after injury. Inflammatory cells in the gut wall respond to FMLP, suggesting a role in post-traumatic stress conditions.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- The mechanisms behind post-injury intestinal mucosal barrier disruption are not fully understood.
- This study investigates the potential role of the bacterial toxin formyl-methionyl leucyl phenylalanine (FMLP) in initiating this disruption.
Purpose of the Study:
- To determine if FMLP contributes to increased intestinal mucosal permeability.
- To explore the involvement of mast cells and other inflammatory cells in FMLP-induced barrier changes.
Main Methods:
- Measuring mucosal permeability using fluorescein isothiocyanate-labeled dextran in perfused rat ileum.
- Assessing dextran and myeloperoxidase in perfusate following stress surrogates (ischemia/reperfusion, irradiation, TPN).
- Quantifying FMLP recovery and mast cell mediator release (serotonin) in response to FMLP.
Main Results:
- FMLP significantly increased ileal permeability in perfused rats, accompanied by increased myeloperoxidase.
- Ischemia/reperfusion and total parenteral nutrition models also showed increased permeability and inflammation.
- FMLP responsiveness correlated with serotonin release, indicating mast cell involvement, except in irradiated rats.
Conclusions:
- Mast cells and gut-resident inflammatory cells mediate FMLP-induced changes in mucosal permeability.
- Pro-inflammatory mediators in the gut wall may be activated by luminal toxins during traumatic stress.
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