Pteromalus puparum venom impairs host cellular immune responses by decreasing expression of its scavenger receptor gene

Pteromalus puparum venom impairs host cellular immune responses by decreasing expression of its scavenger receptor gene
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Pteromalus puparum 毒液通过降低其清道夫受体基因的表达来损害宿主细胞免疫反应

DOI:
10.1016/j.ibmb.2011.07.001
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发表时间:
2011-11-01
影响因子:
3.8
通讯作者:
Ye, Gongyin
Ye, Gongyin
中科院分区:
农林科学2区
文献类型:
--
作者:
Fang, Qi;Wang, Lei;Ye, Gongyin

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昆虫宿主/寄生虫相互作用是共进化系统,其中宿主防御通过寄生虫机制来平衡,以禁用或隐藏宿主免疫效应器。虽然有丰富的文献对这些系统,寄生虫的免疫功能丧失机制尚未完全阐明。在这里,我们报告了一个新发现的免疫功能丧失机制,在粉蝶/Pteromalus蛹主机/寄生系统。由于毒液注射和寄生抑制宿主的吞噬作用,我们将注意力转向P. raeparum清道夫受体(Pr-SR),提出了P. puparum毒液抑制宿主Pr-SR基因表达的假设。为了验证我们的假设,我们克隆了Pr-SR的全长cDNA,多序列比对表明,推导的氨基酸序列与其他鳞翅目清道夫受体相似。细菌和珠注射诱导Pr-SR mRNA和蛋白质表达,在珠注射后4小时达到峰值。蛇毒注射抑制Pr-SR表达。与浆细胞相比,Pr-SR在粒细胞中特异性表达。我们定位的Pr-SR蛋白质在细胞质和细胞膜,没有证据分泌到宿主血浆。双链RNA设计的Pr-SR mRNA沉默表达的Pr-SR和显着受损的主机吞噬和封装反应。毒液注射同样沉默Pr-SR的表达在第一个8小时后处理,之后的沉默效果逐渐减弱。我们从这些发现中推断,削弱雷帕霉素血细胞免疫反应的一种机制是通过沉默Pr-SR的表达。(C)2011 Elsevier Ltd.保留所有权利。
Insect host/parasitoid interactions are co-evolved systems in which host defenses are balanced by parasitoid mechanisms to disable or hide from host immune effectors. Although there is a rich literature on these systems, parasitoid immune-disabling mechanisms have not been fully elucidated. Here we report on a newly discovered immune-disabling mechanism in the Pieris rapae/Pteromalus puparum host/parasitoid system. Because venom injections and parasitization suppresses host phagocytosis, we turned attention to the P. rapae scavenger receptor (Pr-SR), posing the hypothesis that P. puparum venom suppresses expression of the host Pr-SR gene. To test our hypothesis, we cloned a full-length cDNA of the Pr-SR. Multiple sequences alignment showed the deduced amino acid sequence of Pr-SR is similar to scavenger receptors of other lepidopterans. Bacterial and bead injections induced Pr-SR mRNA and protein expression, which peaked at 4 h post-bead injection. Venom injection inhibited Pr-SR expression. Pr-SR was specifically expressed in granulocytes compared to plasmatocytes. We localized the Pr-SR protein in cytoplasm and cellular membrane, with no evidence of secretion into host plasma. Double-strand RNA designed to Pr-SR mRNA silenced expression of Pr-SR and significantly impaired host phagocytosis and encapsulation reactions. Venom injections similarly silenced Pr-SR expression during the first 8 h post-treatment, after which the silencing effects gradually abated. We infer from these findings that one mechanism of impairing P. rapae hemocytic immune reactions is by silencing expression of Pr-SR. (C) 2011 Elsevier Ltd. All rights reserved.