柞蚕杆状病毒诱导鸡异嗜白细胞脱粒效应的信号转导通路

Signal Pathway Involved in Degranulation of Chicken Heterophil Leucocytes Induced by Antheraea pernyi Baculovirus

通过探讨柞蚕(Antheraea pernyi)杆状病毒诱导鸡异嗜白细胞的信号转导途径,确证其是否具有活化鸡异嗜白细胞的作用。采用β-葡萄糖苷酸酶释放法检测柞蚕杆状病毒诱导的鸡异嗜白细胞脱颗粒反应,并通过应用蛋白酪氨酸激酶(src、syk)、磷脂酰肌醇3-激酶(PI3-K)以及丝裂原活化蛋白激酶(ERK、p38 MAPK、JNK)的特异性抑制剂,分析各蛋白酶通路在柞蚕杆状病毒诱导鸡异嗜白细胞脱粒反应中的作用。结果表明,柞蚕杆状病毒可以显著提高鸡异嗜白细胞的脱粒反应,其中src、PI3-K、JNK的特异性抑制剂能够抑制柞蚕杆状病毒诱导的鸡异嗜白细胞的脱粒反应,而syk、ERK、p38 MARK的特异性抑制剂则对鸡异嗜白细胞脱粒不起作用,说明柞蚕杆状病毒可通过src→PI3-K→JNK信号转导通路来诱导鸡异嗜白细胞的脱粒反应。

In present study, the ability of Antheraea pemyi baculovirus to induce degranulation of chicken heterophil leucocytes was investigated and the relative signal transduction pathway was discussed. The baculo virus-induced degranulation of chicken heterophil leucocytes was evaluated by determining the activity of released β-glucuronidase. Moreover, specific inhibitors were used to investigate the roles of protein tyrosine kinases（src and syk）, phosphatidylinositol 3＇-kinase（ Pl3-K）, and mitogen-activated protein kinases（ERK, p38 MAPK and JNK）. The results showed that baculovirus significantly induced degranulation of chicken heterophil leucocytes. Inhibitors Src, Pl3-K and JNK abolished baculovirus-induced degranulation of chicken heterophil leucocytes, while Syk, ERK and p38 MAPK had no inhibitory effect. Taken together, these findings indicated that Antheraea pernyi baculovirus induced the degranulation of chicken heterophil leucocytes through a src→PI3-K→JNK signal transduction pathway.