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Nonmicrobial Activation of TLRs Controls Intestinal Growth, Wound Repair, and Radioprotection.

William F Stenson1, Matthew A Ciorba1

  • 1Division of Gastroenterology, Washington University School of Medicine, St Louis, MO, United States.

Frontiers in Immunology
|February 8, 2021
PubMed
Summary

Toll-like receptors (TLRs) recognize hyaluronic acid, promoting intestinal growth and repair. This pathway involves TLR4, PGE2, and EGFR, crucial for epithelial stem cell proliferation and radioprotection.

Keywords:
LGR5+ epithelial stem cellPGE2TLR4epidermal growth Factor receptor (EGFR)hyaluronic acidintestinal growthradioprotectionwound repair

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Area of Science:

  • Immunology
  • Gastroenterology
  • Stem Cell Biology

Background:

  • Toll-like receptors (TLRs) are key innate immune sensors, recognizing both microbial and non-microbial molecules.
  • Hyaluronic acid, an extracellular matrix component, is recognized by TLR2 and TLR4.
  • Endogenous hyaluronic acid binding to TLR4 is essential for neonatal intestinal growth.

Purpose of the Study:

  • To elucidate the role of hyaluronic acid-TLR4 signaling in intestinal development and repair.
  • To investigate the mechanisms of epithelial proliferation in response to TLR activation.
  • To explore the radioprotective effects of TLR agonists in the intestine.

Main Methods:

  • Studies in neonatal mice to assess intestinal growth.
  • Dextran sodium sulfate (DSS) colitis model to study wound repair.
  • Analysis of immune cell migration and cytokine production (e.g., CXCL12, PGE2).
  • Assessment of epithelial stem cell proliferation and apoptosis.

Main Results:

  • Hyaluronic acid-TLR4 signaling drives intestinal growth via PGE2 production and EGFR transactivation in LGR5+ stem cells.
  • A similar pathway involving TLR2/TLR4, CXCL12, and mesenchymal stem cells promotes epithelial proliferation during colitis repair.
  • TLR2 and TLR4 agonists, including hyaluronic acid, protect intestinal stem cells from radiation-induced apoptosis through EGFR-mediated signaling.

Conclusions:

  • Hyaluronic acid-TLR4-EGFR axis is a critical regulator of intestinal development and repair.
  • TLR signaling orchestrates immune cell interactions to promote epithelial regeneration.
  • Targeting TLR pathways offers potential for therapeutic strategies in intestinal injury and radiation protection.