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Related Experiment Video

Updated: Jun 15, 2026

Investigating Intestinal Inflammation in DSS-induced Model of IBD
08:43

Investigating Intestinal Inflammation in DSS-induced Model of IBD

Published on: February 1, 2012

Dipeptidyl peptidase expression during experimental colitis in mice.

Roger Yazbeck1, Melanie L Sulda, Gordon S Howarth

  • 1School of Biological Sciences, Flinders University, Adelaide, South Australia, Australia.

Inflammatory Bowel Diseases
|February 27, 2010
PubMed
Summary

Dipeptidyl peptidase (DP) inhibitors reduce inflammation in dextran sulfate sodium (DSS) colitis by decreasing neutrophil infiltration and preserving regulatory T-cells (Tregs). These findings support DP inhibitors as a potential therapy for inflammatory bowel disease (IBD).

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Area of Science:

  • Gastroenterology
  • Immunology
  • Pharmacology

Background:

  • Previous studies indicated dipeptidyl peptidase (DP) inhibition partially mitigates dextran sulfate sodium (DSS) colitis in mice.
  • This study aimed to elucidate the protective mechanisms of DP inhibition in DSS-induced colitis.

Purpose of the Study:

  • Investigate the role of DP enzymes in DSS colitis.
  • Evaluate the therapeutic potential of DP inhibitors in a preclinical model of inflammatory bowel disease (IBD).

Main Methods:

  • Induce colitis in wildtype (WT) and dipeptidyl peptidase IV knockout (DPIV-/-) mice using 2% DSS.
  • Administer DP inhibitors (Ile-Pyrr-(2-CN)*TFA or Ile-Thia) or saline.
  • Measure DP mRNA and enzyme levels, glucagon-like peptide (GLP)-1 and GLP-2 concentrations, regulatory T-cell (Treg) populations, and neutrophil infiltration (myeloperoxidase assay).

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Last Updated: Jun 15, 2026

Investigating Intestinal Inflammation in DSS-induced Model of IBD
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Effects of Taste Signaling Protein Abolishment on Gut Inflammation in an Inflammatory Bowel Disease Mouse Model
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Main Results:

  • DP expression and activity were altered in the colon during DSS colitis.
  • DP inhibitors significantly reduced neutrophil infiltration and increased GLP-1 and GLP-2 levels.
  • The Treg population was better maintained in mice treated with DP inhibitors.

Conclusions:

  • DP enzymes play a pathophysiological role in DSS colitis, suggesting involvement in human inflammatory bowel disease (IBD).
  • DP inhibitors demonstrate preclinical efficacy by reducing neutrophil recruitment and supporting Treg populations.
  • Dipeptidyl peptidase IV (DPIV) is critical for the protective effects of DP inhibitors in this colitis model.