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Related Experiment Video

Updated: Jun 26, 2025

Induced Differentiation of M Cell-like Cells in Human Stem Cell-derived Ileal Enteroid Monolayers
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Sorbitol Destroyed Intestinal Microfold Cells (M Cells) Development through Inhibition of PDE4-Mediated RANKL

Li Xiang1,2, Wenxu Pan2, Huan Chen2

  • 1Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, China.

Mediators of Inflammation
|May 10, 2024
PubMed
Summary

Sorbitol inhibits intestinal microfold cell development by downregulating RANKL via PDE4/PKA/CREB signaling. Inhibiting PDE4 with dipyridamole rescues M-cell differentiation, suggesting PDE4 as a target for M-cell induction.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Microfold (M) cells are crucial for intestinal immune surveillance and antigen transport.
  • The precise mechanisms governing M-cell development have remained largely unknown.

Purpose of the Study:

  • To elucidate the mechanism by which sorbitol affects M-cell differentiation.
  • To investigate the role of phosphodiesterase 4 (PDE4) in sorbitol-modulated M-cell development.

Main Methods:

  • Real-time PCR, immunofluorescence, and western blotting were used to assess M-cell differentiation markers.
  • Luciferase assays and chromatin immunoprecipitation identified molecular pathways involved in sorbitol's effects.
  • In vivo and in vitro intestinal models were employed.

Main Results:

  • Sorbitol treatment inhibited M-cell development and enteroid formation, decreasing early and mature M-cell markers.
  • This inhibition was linked to the downregulation of receptor activator of nuclear factor kappa-B ligand (RANKL).
  • Sorbitol upregulated PDE4 phosphorylation, decreasing PKA/CREB activation and leading to reduced RANKL expression.

Conclusions:

  • Sorbitol suppresses intestinal M-cell differentiation and maturation via PDE4-mediated RANKL downregulation.
  • Inhibiting PDE4 can restore M-cell development, highlighting PDE4 as a potential therapeutic target.