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Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
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Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids

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Increased expression of soluble decoy receptor 3 in acutely inflamed intestinal epithelia

Sunghee Kim1, Anastasia Fotiadu, Vassiliki Kotoula

  • 1Department of Biological Sciences, University of Alabama, Rm 280 Nott Hall, Tuscaloosa, AL 35487, USA. skim@bsc.as.ua.edu

Clinical Immunology (Orlando, Fla.)
|May 17, 2005
PubMed

Insights

Decoy receptor 3 (DcR3) release increases in human intestinal cells stimulated by lipopolysaccharide (LPS) via Toll-like receptor 4 (TLR-4) activation. This suggests DcR3 plays a role in intestinal inflammation.

Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • Decoy receptor 3 (DcR3) is a soluble receptor inhibiting apoptosis induced by TNF-family cytokines.
  • Regulation of DcR3 expression is crucial for cellular and tissue homeostasis.
  • Understanding DcR3's role in inflammatory conditions is of significant interest.

Purpose of the Study:

  • To investigate the regulation of DcR3 release in human intestinal epithelial cells (IECs).
  • To explore the signaling pathways involved in DcR3 induction by lipopolysaccharide (LPS).
  • To assess DcR3 expression in acute appendicitis.

Main Methods:

  • Cultured human IEC lines (SW480, SW620, HT29) were stimulated with LPS.
  • Toll-like receptor 4 (TLR-4) expression was assessed.
  • MAPK (ERK1/2, JNK) and NF-kappaB activation pathways were analyzed.
  • DcR3 expression in appendix tissues from appendicitis patients was examined.

Main Results:

  • IEC lines selectively increased DcR3 release upon LPS stimulation.
  • All tested IEC lines expressed TLR-4.
  • LPS-induced DcR3 release involved MAPK and NF-kappaB activation.
  • Increased DcR3 expression was observed in appendix epithelia of appendicitis patients.

Conclusions:

  • Human intestinal epithelial cells increase DcR3 release in response to LPS, mediated by TLR-4, MAPK, and NF-kappaB.
  • DcR3 may play a significant role in the human intestinal epithelium during endotoxin-induced acute inflammatory processes.
  • These findings highlight DcR3's potential involvement in inflammatory bowel diseases.

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