Effect of prednisone on IL-17 secretion in maternal-fetal immune rejection cell model, and on IL-23/IL-17 inflammation axis

Purpose: To investigate the influence of prednisone on secretion of IL-17 in maternal-fetal immune rejection cell model, and on tIL-23/IL-17 inflammation axis. Methods: Four groups of Kunming mice were used. Group A was given blank culture solution. Group B was first given prednisone; thereafter, TGF-β, IL-23, and IL-6 were added. Groups C and D were first treated with culture solution containing TGF-β, IL-23, and IL-6. Then, prednisone was added to group C, while blank culture solution was added to group D. The mRNA expressions of IL-23 and IL-17 in mouse spleen lymphocytes were assayed in the four groups using their respective culture supernatants. Results: The IL-17 concentration was significantly downregulated in group B, relative to the other groups (p < 0.05). Expression of IL-17 mRNA in mouse spleen lymphocytes was significantly downregulated in group B, when compared to the other groups, and was also higher in groups A and D than in group C (p < 0.05). After cytokine stimulation, IL-17 and IL-23 were upregulated in groups C and D. The expression level of mRNA was higher in D than in C (p < 0.05). Conclusion: Prednisone inhibits the proliferation of lymphocytes. During immune imbalance, prednisone regulates immunity by controlling the secretion of IL-17 via downregulation of the expressions of genes for pro-inflammatory factors IL-17 and IL-23.

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