首页> 外文OA文献 >Modulation of immune responses of Rhynchophorus ferrugineus (Insecta: Coleoptera) induced byudthe entomopathogenic nematode Steinernema carpocapsae (Nematoda: Rhabditida).
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Modulation of immune responses of Rhynchophorus ferrugineus (Insecta: Coleoptera) induced byudthe entomopathogenic nematode Steinernema carpocapsae (Nematoda: Rhabditida).

机译:ud诱导的对Rhynchophorus ferrugineus(Insecta:Coleoptera)免疫应答的调节昆虫病原线虫Steinernema carpocapsae(线虫:Rhabditida)。

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摘要

Aim of this study was to investigate relationships between the red palm weevil (RPW)udRhynchophorus ferrugineus (Olivier) and the entomopathogenic nematode Steinernema carpocapsaeud(EPN); particularly, the work was focused on the immune response of the insect host in naive larvae andudafter infection with the EPN. Two main immunological processes have been addressed: the activity andudmodulation of host prophenoloxidase-phenoloxidase (proPO) system, involved in melanization of not-selfudand hemocytes recognition processes responsible for not-self encapsulation. Moreover, immune depressiveudand immune evasive strategies of the parasite have been investigated. Our results suggest that RPWudpossess an efficient immune system, however in the early phase of infection, S. carpocapsae induces audstrong inhibition of the host proPO system. In addition, host cell-mediated mechanisms of encapsulation,udare completely avoided by the parasite, the elusive strategies of S. carpocapsae seem to be related to theudstructure of its body-surface, since induced alterations of the parasite cuticle resulted in the loss of its mimetic properties. S. carpocapsae before the release of its symbiotic bacteria, depress and elude RPWudimmune defenses, with the aim to arrange a favorable environment for its bacteria responsible of theudsepticemic death of the insect target.
机译:本研究的目的是调查红掌象鼻虫(RPW) udRhynchophorus ferrugineus(Olivier)与昆虫病原线虫Steinernema carpocapsae ud(EPN)之间的关系;特别是,这项工作的重点是幼虫和EPN感染后昆虫宿主对幼虫的免疫反应。已经解决了两个主要的免疫学过程:宿主酚氧化酶-酚氧化酶(proPO)系统的活性和调制,参与负责非自身包囊的非自身和血细胞识别过程的黑色素化。此外,已经研究了该寄生虫的免疫抑制/免疫逃避策略。我们的结果表明RPW具有有效的免疫系统,但是在感染的早期阶段,糖荚膜链球菌诱导了对宿主proPO系统的强烈抑制。此外,寄生虫完全避免了宿主细胞介导的包囊机制,炭疽链球菌的难以捉摸的策略似乎与其体表的结构有关,因为寄生虫表皮的诱导改变导致失去其模拟特性。炭疽链球菌在其共生细菌释放之前,压制并逃避了RPW udimmune防御,目的是为其细菌造成昆虫靶标的败血症死亡提供有利的环境。

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