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