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Chronic Pancreatitis II: Pathophysiology01:21

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Protocols for Analyzing the Role of Paneth Cells in Regenerating the Murine Intestine using Conditional Cre-lox Mouse Models
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Starvation compromises Paneth cells.

Caroline M Hodin1, Kaatje Lenaerts, Joep Grootjans

  • 1Department of Surgery, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center, Maastricht, The Netherlands.

The American Journal of Pathology
|October 12, 2011
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Summary

Food deprivation impairs Paneth cells, crucial for gut immunity. This leads to increased intestinal permeability and bacterial translocation, potentially explaining high mortality in starved patients.

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Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Lack of enteral feeding increases intestinal permeability and bacterial translocation.
  • Paneth cells are key components of innate intestinal immunity, protecting against bacterial invasion.
  • Bacterial translocation contributes to high morbidity and mortality in patients on nil by mouth orders.

Purpose of the Study:

  • To investigate the impact of food deprivation on Paneth cell function in a mouse starvation model.
  • To understand the role of Paneth cell dysfunction in bacterial translocation during starvation.

Main Methods:

  • Utilized a mouse starvation model.
  • Performed quantitative PCR to assess antimicrobial gene expression.
  • Conducted Western blot analysis and immunohistochemistry (IHC) for protein expression.
  • Employed electron microscopy to examine Paneth cell ultrastructure.
  • Quantified bacterial translocation to mesenteric lymph nodes.

Main Results:

  • 48 hours of food deprivation significantly decreased mRNA expression of Paneth cell antimicrobials (lysozyme, cryptdin, RegIIIγ).
  • Protein levels of lysozyme and RegIIIγ precursor were also diminished.
  • Electron microscopy revealed degenerative autophagolysosomes and aberrant granules in Paneth cells.
  • Increased bacterial translocation to mesenteric lymph nodes was observed, correlating with Paneth cell abnormalities.

Conclusions:

  • Enteral starvation induces Paneth cell abnormalities, including reduced antimicrobial production and ultrastructural changes.
  • These Paneth cell alterations may compromise epithelial barrier function.
  • The observed changes likely contribute to bacterial translocation during enteral starvation.