OBJECTIVE: The aim of this study was to investigate the mechanisms of miR-138 in regulating Th2 type immune response by targeting OX40 ligand (Ox40L) in vitro. METHODS: Serum samples of patients were used to explore the clinical parameter. Wistar rats were used to establish a murine model of asthma. The dual-luciferase report assay was used to detect the regulation of miR-138 on the expression of OX40L. RT-PCR was used to detect miR-138 and OX40L mRNA expression. Mixed lymphocyte reaction (MLR) and Western blot were used to analyze target protein expression. Enzyme linked immune sorbent assay (ELISA) and flow cytometry (FCM) were used to cytokines detection. RESULTS: The level of miR-138 was found to be negatively correlated with the expression of OX40L (P < 0.05) and positively correlated with FEV1 (P < 0.05). Higher miR-138 and reduced expression of OX40L were observed in dendritic cells (DCs) separated from rat bone marrow. Typically, OX40 and OX40L in asthma group were determined and the results indicated that the two parameters upregulated in compared with healthy control, while the expressions of them were suppressed by over-expression of miR-138. Furthermore, the up-regulation of Th1 cytokines (IL-2 and IFN-γ) and the down-regulation of Th2 cytokines (IL-4 and IL-10) were induced by over-expression miR-138 and meanwhile the decrease of Th1/Th2 was reversed by overexpression of miR-138. CONCLUSION: In this study, we revealed that miR-138 might regulate Th2-type immune response by down-regulating the OX40L expression in asthma. IJCEP
OBJECTIVE: The aim of this study was to investigate the mechanisms of miR-138 in regulating Th2 type immune response by targeting OX40 ligand (Ox40L) in vitro. METHODS: Serum samples of patients were used to explore the clinical parameter. Wistar rats were used to establish a murine model of asthma. The dual-luciferase report assay was used to detect the regulation of miR-138 on the expression of OX40L. RT-PCR was used to detect miR-138 and OX40L mRNA expression. Mixed lymphocyte reaction (MLR) and Western blot were used to analyze target protein expression. Enzyme linked immune sorbent assay (ELISA) and flow cytometry (FCM) were used to cytokines detection. RESULTS: The level of miR-138 was found to be negatively correlated with the expression of OX40L (P < 0.05) and positively correlated with FEV1 (P < 0.05). Higher miR-138 and reduced expression of OX40L were observed in dendritic cells (DCs) separated from rat bone marrow. Typically, OX40 and OX40L in asthma group were determined and the results indicated that the two parameters upregulated in compared with healthy control, while the expressions of them were suppressed by over-expression of miR-138. Furthermore, the up-regulation of Th1 cytokines (IL-2 and IFN-γ) and the down-regulation of Th2 cytokines (IL-4 and IL-10) were induced by over-expression miR-138 and meanwhile the decrease of Th1/Th2 was reversed by overexpression of miR-138. CONCLUSION: In this study, we revealed that miR-138 might regulate Th2-type immune response by down-regulating the OX40L expression in asthma. IJCEP