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Cytokine-stimulated release of decay-accelerating factor (DAF;CD55) from HT-29 human intestinal epithelial cells
1First Department of Internal Medicine, Okayama University Medical School, Japan.
Clinical and Experimental Immunology
|September 16, 1998
Summary
Interleukin-4 and Interleukin-1beta cytokines significantly increase the release of Decay Accelerating Factor (DAF) from intestinal cells. This suggests these cytokines may play a role in DAF release observed in ulcerative colitis patients.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Decay Accelerating Factor (DAF, CD55) expression is elevated in ulcerative colitis (UC) patients.
- Cytokines influence DAF expression, and UC lesions show altered cytokine profiles.
Purpose of the Study:
- To investigate the effects of various cytokines on DAF synthesis and release in HT-29 intestinal epithelial cells.
- To determine the role of specific cytokines in DAF modulation relevant to UC.
Main Methods:
- Utilized flow cytometry and ELISA to quantify DAF expression and release.
- Treated HT-29 cells with cytokines (IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IFN-gamma).
- Assessed DAF release kinetics and inhibition using Actinomycin D, cycloheximide, and brefeldin A.
Main Results:
- HT-29 cells constitutively express and release both cell-surface bound and soluble DAF.
- Interleukin-4 (IL-4) markedly and Interleukin-1beta (IL-1beta) moderately enhanced DAF expression and release.
- Inhibitors blocked IL-4 and IL-1beta-induced DAF release, indicating a requirement for de novo synthesis.
Conclusions:
- DAF is released from intestinal epithelial cells upon cytokine stimulation.
- IL-4 and IL-1beta are key cytokines potentially driving DAF release into the colonic lumen in UC patients.