Keywords:Biotechnology Essay 代写
据报道，IV可以激活IL-22的表达。最初，我们研究的是流感病毒感染在发病中的表达调控作用。探讨IL-22和IL-34诱导动力学，测定不同时间点与病毒在感染复数感染后的mRNA及蛋白表达IL-22和IL-34（MOI）1。流感病毒感染健康人新鲜分离的外周血单个核细胞导致增加IL-22和IL-34 mRNA和蛋白的表达（图2A）。IL-22和IL-34 mRNA水平增加早在感染后24小时和IL-22和发病水平持续在整个实验过程中增加。IL-22和发病水平呈现类似的趋势，以ELISA法测定分析（图2C）。我们的下一个被感染的新鲜分离的PBMCs与不同剂量的流感病毒，收获细胞，感染后48小时。IL-22和IL-34 mRNA水平与IAV剂量呈正相关（图2B）。在ELISA中IL-22和IL-34蛋白水平分析反映的转录数据（图2D）。这些结果表明，IAV感染可激活一次，IL-34表达IL-22和剂量依赖的方式。 确定IL-22在发病中的mRNA和蛋白水平的激活效应，新鲜分离的外周血单个核细胞转染RNAi质粒IL-22量不同。结果表明，抑制IL-22抑制IAV的IL-34诱导活化（图3d）。此外，培养上清液中的发病是由生产IL-22的RNAi质粒以剂量依赖的方式抑制（图3E）。总之，这些数据表明IL-22是IAV的上游调控因子IL-34生产引发。
It has been reported that IV can activate the expression of IL-22. Initially, we investigated whether IAV infection played a role in the regulation of IL-34 expression. To explore the kinetics of IL-22 and IL-34 induction, both mRNA and protein expression of IL-22 and IL-34 were measured at various time points after infection with IAV at a multiplicity of infection (MOI) of 1. IAV infection of freshly isolated PBMCs from healthy individuals resulted in increased IL-22 and IL-34 mRNA and protein expressions (Fig. 2A). The mRNA levels of IL-22 and IL-34 was increased as early as 24 hours after infection and IL-22 and IL-34 levels continued to increase throughout the course of the experiment. IL-22 and IL-34 levels showed a similar trend as determined by ELISA analyses (Fig. 2C). We next infected freshly isolated PBMCs with various doses of IAV and harvested the cells 48 hours after infection. IL-22 and IL-34 mRNA levels were positively correlated with the doses of IAV (Fig. 2B). Protein levels of IL-22 and IL-34 in ELISA analyses mirrored the transcription data (Fig. 2D). These results suggested that IAV infection could activate the expression of IL-22 and IL-34 in a time- and dose- dependent manner.
To determine the effects of IL-22 on the activation of IL-34 mRNA level and protein expression, freshly isolated PBMCs transfected with different amounts of RNAi plasmids for IL-22. The result showed that knockdown of IL-22 inhibited IAV-induced activation of the IL-34 (Fig. 3D). Furthermore, IL-34 production in culture supernatants was inhibited by IL-22 RNAi plasmids in a dose-dependent manner (Fig. 3E). Taken together, these data suggested that IL-22 was an upstream regulatory factor of IAV-triggered IL-34 production.