首页> 中文期刊> 《动物医学进展》 >马链球菌对树突状细胞 Toll 样受体和 MyD88及细胞因子 mRNA 表达的影响

马链球菌对树突状细胞 Toll 样受体和 MyD88及细胞因子 mRNA 表达的影响

         

摘要

为探究马链球菌马亚种(Streptococcus equi subsp.equi,S.equi)对小鼠骨髓源树突状细胞(bone marrow derived dendritic cells,BMDCs)TLR1、TLR2、TLR6、MyD88、IL-1、IL-6、IL-10、IL-12、TNF-αmRNA 表达的影响,用 GM-CSF、IL-4细胞因子刺激小鼠骨髓细胞使其诱导分化成未成熟的 BMDCs,感染 S.equi 后16、20、26 h,采用 SYBR Green Ⅰ实时荧光定量 PCR 检测感染组及未感染组细胞 TLRs、MyD88和细胞因子 mRNA 的表达情况。结果显示,S.equi 感染 BMDCs 后16、20、26 h,TLR1、TLR2、TLR6、MyD88 mRNA 的表达量均显著或极显著的高于未感染组(P <0.05或 P <0.01)。S.equi 感染 DCs后16、26 h,IL-1的分泌量较未感染组没有变化(P >0.05),IL-10、TNF-α的分泌量显著或极显著增加(P <0.05或 P <0.01)。IL-6在 S.equi 感染 DCs 后16 h 的分泌量显著增加(P <0.05),但感染后26 h 无显著变化(P >0.05)。IL-12在 S.equi 感染 DCs 后16 h 的表达没有变化(P >0.05),但感染后26 h 分泌量有所增加(P <0.05)。说明 S.equi 具有调节 DCs TLRs、MyD88和细胞因子表达的能力,从而介导机体的免疫应答反应。%To study the effects of Streptococcus equi subsp equi (S.equi )on the mRNA expressions of TLR1,TLR2,TLR6,MyD88,IL-1,IL-6,IL-10,IL-12 and TNF-α in mouse bone marrow derived dendritic cells (BMDCs)cultured in vitro ,Naive DCs were cultured with GM-CSF and IL-4,SYBR Green Ⅰfluores-cence quantitative PCR was used to detect mRNA transcriptional levels of TLRs,MyD88 and cytokines af-ter infection with S.equi about 16,20,26 h.The results showed that at 16,20,26 h post-infections,the ex-pression levels of TLR1,TLR2,TLR6 and MyD88 in S.equi infected BMDCs were significantly or ex-tremely significantly higher than those of the negative control group (P <0.05 or P <0.01 ).At 16,26 h post-infections,the concentration of IL-1 had no obviously change (P >0.05),IL-10,TNF-α were signifi-cantly or extremely significantly increased than those of the negative control group (P <0.05 or P <0.01). IL-6 was significantly increased at 16 h post-infection (P <0.05),however,it had no change at 26 h post-infection (P > 0.05).At 16 h post-infection,the concentration of IL-12 had no obviously change (P >0.05),while at 26 h post-infection,it was significantly increased (P <0.05).These results indicated that S.equi was able to regulate the mRNA expressions of TLRs,MyD88 and cytokines,which mediated im-mune responses.

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