Tang Ting, Li Wenqian, Wang Xiaofen, Wu Yinjian, Liu Fengsong
The Key Laboratory of Zoological Systematics and Application, College of Life Sciences, Hebei University, Baoding, Hebei, 071002, China.
The Key Laboratory of Zoological Systematics and Application, College of Life Sciences, Hebei University, Baoding, Hebei, 071002, China.
Dev Comp Immunol. 2019 Jan;90:21-28. doi: 10.1016/j.dci.2018.08.016. Epub 2018 Aug 27.
In mammals, the TNF family is important inflammatory cytokines. Eiger, the invertebrate ortholog of TNF identified firstly in Drosophila, has been implicated in immune response with an unknown molecular mechanism. The present work reports a novel eiger like gene (Mdeiger) from Musca domestica. Mdeiger was significantly up-regulated upon challenge with either Escherichia coli or Staphylococcus aureus. Silencing Mdeiger led to higher mortalities of larvae post either E. coli or S. aureus infection, enhanced the expressions of attacin and diptericin, but blocked the induction of ceropin and muscin, and inhibited the activation of phenoloxidase following bacterial challenge. Meanwhile, the expression of dorsal and JNK was inhibited while that of relish was enhanced in Mdeiger-depleted larvae. We suppose that, by coordinating with the Imd, Toll and JNK pathways, Mdeiger be involved in regulating the innate immune response through controlling the capacity of phenoloxidase and the expression of antimicrobial peptide genes synergistically.
在哺乳动物中，肿瘤坏死因子（TNF）家族是重要的炎性细胞因子。艾格（Eiger）是首先在果蝇中鉴定出的TNF无脊椎动物直系同源物，它参与免疫反应，但其分子机制尚不清楚。目前的研究报告了家蝇中一个新的类艾格基因（Mdeiger）。在用大肠杆菌或金黄色葡萄球菌攻击后，Mdeiger显著上调。沉默Mdeiger会导致大肠杆菌或金黄色葡萄球菌感染后幼虫的死亡率更高，增强了抗菌肽attacin和双翅肽的表达，但阻断了杀菌肽和家蝇抗菌肽的诱导，并抑制了细菌攻击后酚氧化酶的激活。同时，在缺失Mdeiger的幼虫中，背侧蛋白和JNK的表达受到抑制，而 relish的表达增强。我们推测，通过与免疫缺陷（Imd）、Toll和JNK信号通路协同作用，Mdeiger通过协同控制酚氧化酶的活性和抗菌肽基因的表达来参与调节先天免疫反应。
