AIM: To investigate the effects of butyrate on interleukin (IL)-32alpha expression in epithelial cell lines. METHODS: The human intestinal epithelial cell lines HT-29, SW480, and T84 were used. Intracellular IL-32alpha was determined by Western blotting analyses. IL-32alpha mRNA expression was analyzed by real-time polymerase chain reaction. RESULTS: Acetate and propionate had no effects on IL-32alpha mRNA expression. Butyrate significantly enhanced IL-32alpha expression in all cell lines. Butyrate also up-regulated IL-1beta-induced IL-32alpha mRNA expression. Butyrate did not modulate the activation of phosphatidylinositol 3-kinase (PI3K), a mediator of IL-32alpha expression. Like butyrate, trichostatin A, a histone deacetylase inhibitor, also enhanced IL-1beta-induced IL-32alpha mRNA expression. CONCLUSION: Butyrate stimulated IL-32alpha expression in epithelial cell lines. An epigenetic mechanism, such as histone hyperacetylation, might be involved in the action of butyrate on IL-32alpha expression.
AIM: To investigate the effects of butyrate on interleukin (IL)-32alpha expression in epithelial cell lines. METHODS: The human intestinal epithelial cell lines HT-29, SW480, and T84 were used. Intracellular IL-32alpha was determined by Western blotting analyses. IL-32alpha mRNA expression was analyzed by real-time polymerase chain reaction. RESULTS:Acetate and propionate had no effects on IL-32alpha mRNA expression. Butyrate significantly enhanced IL-32alpha expression in all cell lines. Butyrate also up-regulated IL-1beta-induced IL-32alpha mRNA expression. Butyrate did not modulate the activation of phosphatidylinositol 3-kinase (PI3K), a mediator of IL-32alpha expression. Like butyrate, trichostatin A, a histone deacetylase inhibitor, also enhanced IL-1beta-induced IL-32alpha mRNA expression. CONCLUSION:Butyrate stimulated IL-32alpha expression in epithelial cell lines. An epigenetic mechanism, such as histone hyperacetylation, might be involved in the action of butyrate on IL-32alpha expression.
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