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Induction of Paneth cell degranulation by orally administered Toll-like receptor ligands

Cristiano Rumio1, Michele Sommariva, Lucia Sfondrini

  • 1Department of Human Morphology and Biomedical Sciences Città Studi University of Milan, Milan, Italy.

Journal of Cellular Physiology
|May 14, 2011
PubMed

Insights

Toll-like receptor (TLR) 9 and TLR3 agonists trigger Paneth cell degranulation, crucial for intestinal immunity. This discovery offers new pathways for treating inflammatory bowel diseases and infections.

Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Paneth cells in the small intestine secrete enzymes and antimicrobial peptides, influenced by gut bacteria.
  • The specific molecular triggers for Paneth cell secretion remain incompletely understood.

Purpose of the Study:

  • To investigate the role of Toll-like receptors (TLRs) in mediating Paneth cell secretory responses.
  • To identify specific TLR agonists that induce Paneth cell degranulation.

Main Methods:

  • Oral administration of Toll-like receptor agonists (CpG-ODN, polyinosinic-polycytidylic acid, LPS, flagellin) to mice.
  • Utilized knockout mice (TLR9-/-) and bone marrow chimeric mice to determine the cellular source of TLR recognition.
  • Assessed Paneth cell degranulation and inflammatory mediator production (TNF-α).

Main Results:

  • CpG-oligodeoxynucleotide (ODN), a TLR9 agonist, induced rapid Paneth cell degranulation in wild-type mice.
  • TLR9-expressing gastrointestinal cells were identified as critical for CpG-ODN recognition.
  • The TLR3 agonist polyinosinic-polycytidylic acid also caused rapid degranulation, while TLR4 and TLR5 agonists induced delayed degranulation via TNF-α.

Conclusions:

  • TLR9 and TLR3 agonists are potent inducers of Paneth cell degranulation.
  • Understanding these TLR-mediated pathways is essential for developing strategies against intestinal infections and inflammatory bowel diseases.

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