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Sterile inflammation drives multiple programmed cell death pathways in the gut.

Carolina N Ruera1, Emanuel Miculán1, Federico Pérez1

  • 1Departamento de Ciencias Biológicas, Facultad de Ciencias Exactas, Instituto de Estudios Inmunológicos y Fisiopatológicos (IIFP), UNLP, CONICET, associated to CIC PBA, La Plata, Argentina.

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|September 18, 2020
PubMed
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Inflammation in the small intestine triggers multiple programmed cell death (PCD) pathways, including apoptosis, pyroptosis, and necroptosis, in intestinal epithelial cells. This study reveals these diverse cell death mechanisms during p31-43 gliadin peptide-induced enteropathy in mice.

Keywords:
celiac diseaseinflammationinnate immunityprogrammed cell deathsmall intestine

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Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Intestinal epithelial cells undergo rapid turnover, involving programmed cell death (PCD) to remove damaged cells.
  • Apoptosis is the primary PCD pathway in healthy intestines, but mechanisms during inflammation remain unclear.
  • Pyroptosis and necroptosis are inflammatory PCD forms that activate innate immune responses.

Purpose of the Study:

  • To investigate the specific programmed cell death (PCD) pathways activated during p31-43 gliadin peptide-induced enteropathy.
  • To understand the role of different PCD mechanisms in intestinal inflammation and damage.

Main Methods:

  • Utilized an in vivo mouse model of enteropathy induced by p31-43 gliadin peptide.
  • Employed TUNEL staining, Western blot, and immunofluorescence to detect cell death markers.
  • Assessed pyroptosis activation via caspase-1, IL-1β, and gasdermin D.
  • Investigated necroptosis by examining RIPK3 expression.

Main Results:

  • p31-43 administration rapidly increased TUNEL-positive cells, indicating widespread cell death.
  • Caspase-3 mediated apoptosis was confirmed in the intestinal epithelium and lamina propria.
  • Evidence of pyroptosis activation (mature caspase-1, IL-1β, gasdermin D) and necroptosis (RIPK3 up-regulation) was observed.
  • Inhibiting caspase-1 reduced enterocyte death, highlighting pyroptosis's contribution.

Conclusions:

  • The p31-43 gliadin peptide induces multiple programmed cell death pathways in the small intestine during inflammation.
  • Apoptosis, pyroptosis, and necroptosis contribute to intestinal epithelial cell removal in this inflammatory model.
  • Understanding these diverse PCD pathways is crucial for managing inflammatory enteropathies.