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Related Experiment Video

Updated: May 31, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Published on: April 21, 2015

TRPA1 and substance P mediate colitis in mice.

Matthias A Engel1, Andreas Leffler, Florian Niedermirtl

  • 1Institute of Physiology and Pathophysiology, First Department of Medicine, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.

Gastroenterology
|July 19, 2011
PubMed
Summary
This summary is machine-generated.

The irritant receptor TRPA1 (transient receptor potential of the ankyrin type-1) and substance P play key roles in causing and sustaining colitis. Inhibiting TRPA1 or blocking substance P can reduce intestinal inflammation in mice.

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Area of Science:

  • Neuroscience
  • Gastroenterology
  • Immunology

Background:

  • Neuropeptides calcitonin gene-related peptide (CGRP) and substance P are implicated in experimental colitis.
  • Calcium channels regulate the release of these neuropeptides from sensory neurons.

Purpose of the Study:

  • Investigate the mechanisms of colitis in two models.
  • Determine the involvement of the irritant receptor TRPA1 (transient receptor potential of the ankyrin type-1).
  • Elucidate the effects of CGRP and substance P in colitis.

Main Methods:

  • Utilized calcium-imaging, patch-clamp, and neuropeptide-release assays.
  • Induced colitis using 2,4,6-trinitrobenzene-sulfonic-acid (TNBS) and dextran-sulfate-sodium-salt in wild-type, knockout, and desensitized mice.

Main Results:

  • TNBS triggered TRPA1-dependent release of substance P and CGRP, calcium influx, and sustained currents in neurons.
  • TNBS covalently bound to TRPA1, potentially leading to sustained sensitization via sulfinic acid transformation.
  • Colitis was reduced in TRPA1 knockout mice and with a TRPA1 inhibitor; substance P was found to be proinflammatory.
  • Inflammatory lipid peroxidation products also induced TRPA1-dependent neuropeptide release.

Conclusions:

  • Neuroimmune interactions are critical in controlling intestinal inflammation.
  • Activation and sensitization of TRPA1, along with substance P release, are key drivers in the induction and maintenance of colitis.