抑制p38MAPK信号通路对Bpiv3复制的影响

由牛副流感病毒3型(Bovine parainfluenza virus type 3,Bpiv3)感染引起的牛副流感病已成为各国牛场最重要的传染病之一,每年都会给世界养牛业造成巨大的经济损失,但关于该病致病的分子机制研究较少。本研究通过观察Bpiv3感染对MDBK细胞中丝裂原活化蛋白激酶(MKK3)及其下游分子p38丝裂酶原活化的蛋白激酶(p38MAPK)的表达的影响,探讨相关的信号转导机制,对p38 MAPK通路在Bpiv3感染过程中的作用进行了初步研究。Bpiv3感染细胞后,采用Western Blot检测MKK3,p38 MAPK在蛋白水平的表达变化,并采用ELISA法检测细胞上清中IL-6,IL-8,IL-13和TNF-α的水平变化,采用SPSS 12软件进行统计学分析。结果表明,Bpiv3在感染后能够诱导MKK3的激活以及p38的磷酸化,激活了p38 MAPK信号通路。而且p38 MAPK信号通路参与了Bpiv3的复制过程。ELISA检测Bpiv3感染后以及使用抑制剂SB202190处理后的细胞上清中IL-6、IL-8、IL-13和TNF-α的水平发现,p38 MAPK信号通路参与了Bpiv3诱导的炎症反应。研究证实Bpiv3感染能够激活p38 MAPK通路,显著上调MKK3的表达并诱导p38发生磷酸化,进一步激活下游分子发挥生物学活性,促进Bpiv3的复制及诱导促炎细胞因子的产生。p38 MAPK信号通路的激活可能是Bpiv3感染诱发炎症反应的机制之一。

The Role of the p38 MAPK Signaling Pathway in Bpiv3 Replication

The bovine parainfluenza 3 virus( Bpiv3) can cause economic losses in the cattle industry. However,research on the molecular mechanism of the Bpiv3 infection are rarely reported. We measured expression of MKK3 and p38 mitogen-activated protein kinase( MAPK) after Bpiv3 infection. The signal-transduction mechanism of Bpiv3 infection was investigated, and the effect of the p38 MAPK pathway upon Bpiv3 infection was studied in a preliminary fashion. Expression of MKK3 and p38 MAPK was measured by Western Blot. The level of interleukin(IL)-6, IL-8, IL-13 and tumor necrosis factor(TNF)-α were tested by ELISA. Data were analyzed with SPSS 12. Results showed that Bpiv3 could induce activation of MKK3 and phosphorylation of p38 after infection. Bpiv3 infection could activate the p38 MAPK signaling pathway, and the latter, was involved in Bpiv3 replication. Levels of IL-6, IL-8, IL-13 and TNF-α, suggested that the p38 MAPK signaling pathway participated in the response to the inflammation caused by Bpiv3 infection. Activation of the p38 MAPK signaling pathway may be one of the mechanisms of inflammation induced by Bpiv3 infection.