Related Experiment Videos
Tumour necrosis factor-alpha up-regulates decay-accelerating factor gene expression in human intestinal epithelial
A Andoh1, Y Fujiyama, K Sumiyoshi
1Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan.
Immunology
|March 1, 1997
Summary
Tumor necrosis factor-alpha (TNF-α) significantly increases decay-accelerating factor (DAF) mRNA and protein in intestinal cells. This suggests TNF-α plays a key role in regulating DAF at inflamed mucosal sites.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Increased decay-accelerating factor (DAF) expression is observed in intestinal epithelial cells at inflamed mucosal sites.
- Tumor necrosis factor-alpha (TNF-α) is a key inflammatory cytokine implicated in mucosal inflammation.
Purpose of the Study:
- To investigate the effects of TNF-α on DAF expression in human intestinal epithelial cell lines.
- To elucidate the mechanisms by which TNF-α regulates DAF expression.
Main Methods:
- Utilized three human intestinal epithelial cell lines (HT-29, T84, Caco-2).
- Assessed DAF mRNA levels via Northern blot analysis.
- Quantified DAF protein expression using biotin labeling and immunoprecipitation.
Main Results:
- TNF-α markedly increased both DAF mRNA and protein expression in all tested cell lines.
- The TNF-α effect on DAF mRNA was dose-dependent and time-limited, peaking at 3-6 hours.
- Regulation of DAF expression by TNF-α involved de novo protein synthesis and post-transcriptional mechanisms, including mRNA stability.
- Interleukin-4 (IL-4) combined with TNF-α showed additive effects on DAF mRNA accumulation.
Conclusions:
- TNF-α is a potent inducer of DAF mRNA expression in human intestinal epithelial cells.
- TNF-α plays a significant role in regulating DAF expression, particularly at inflamed mucosal sites.
- These findings highlight a potential mechanism linking inflammation and complement regulation in the gut.