Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2017
MiR-146a overexpression effectively improves experimental allergic conjunctivitis through regulating CD4+CD25-T cells.
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Yang Yang, Yin Xiaolong, Yi Jinglin, Peng Xiaowei
Аннотация
OBJECTIVE: To study the mechanism of miR-146a in the regulation of allergic conjunctivitis (AC) through CD4+CD25-T cells.
METHODS: BALB/c mice were sensitized with ragweed pollen (RW) and alum, and then challenged with RW. Eosinophil infiltration was determined using Giemsa assay. ELISA assay was performed to examine the level of antigen-specific IgE in the serum and cytokine levels in splenocytes. The expression of miR-146a was measured by qRT-PCR. Flow cytometric analysis was used to analyze the percentage of CD4+CD25-T cells and Tregs.
RESULTS: In this study, we found that miR-146a overexpression could effectively improve the symptoms of AC in mouse models. Moreover, in vitro experiments, the proliferation of splenocytes was controlled and the expression of IL-5 and IL-13 was also decreased after transfected with miR-146a mimic. In addition, the inhibitory effect of Tregs on Tcons was affected by the change of miR-146a content in Tcons and had a positive correlation effect. When the content of miR-146a in Tregs changed, the inhibition was not affected. In addition, when inhibited miR-146a, NF-κB signaling pathway was activated, and the expression of IL-5 and IL-13 in Tcons increased. While after added Bay (NF-κB blocker), the NF-κB activity was decreased, and the expression of IL-5 and IL-13 in Tcons also reduced.
CONCLUSION: MiR-146a decreased in Tcons was contributed to the development of AC through regulating the inhibitory effect of Tregs on Tcons and NF-κB signaling pathway.
METHODS: BALB/c mice were sensitized with ragweed pollen (RW) and alum, and then challenged with RW. Eosinophil infiltration was determined using Giemsa assay. ELISA assay was performed to examine the level of antigen-specific IgE in the serum and cytokine levels in splenocytes. The expression of miR-146a was measured by qRT-PCR. Flow cytometric analysis was used to analyze the percentage of CD4+CD25-T cells and Tregs.
RESULTS: In this study, we found that miR-146a overexpression could effectively improve the symptoms of AC in mouse models. Moreover, in vitro experiments, the proliferation of splenocytes was controlled and the expression of IL-5 and IL-13 was also decreased after transfected with miR-146a mimic. In addition, the inhibitory effect of Tregs on Tcons was affected by the change of miR-146a content in Tcons and had a positive correlation effect. When the content of miR-146a in Tregs changed, the inhibition was not affected. In addition, when inhibited miR-146a, NF-κB signaling pathway was activated, and the expression of IL-5 and IL-13 in Tcons increased. While after added Bay (NF-κB blocker), the NF-κB activity was decreased, and the expression of IL-5 and IL-13 in Tcons also reduced.
CONCLUSION: MiR-146a decreased in Tcons was contributed to the development of AC through regulating the inhibitory effect of Tregs on Tcons and NF-κB signaling pathway.