Contrasting infection strategies in generalist and specialist wasp parasitoids of Drosophila melanogaster.
Contrasting infection strategies in generalist and specialist wasp parasitoids of Drosophila melanogaster.
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DOI：
10.1371/journal.ppat.0030158
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发表时间：
2007-10-26
期刊：
影响因子：
6.7
通讯作者：
Clark AG
中科院分区：
文献类型：
--
作者：
Schlenke TA;Morales J;Govind S;Clark AG
虽然宿主-寄生蜂相互作用在生物体和细胞水平上得到了很好的表征，但宿主免疫反应的分子基础和寄生蜂击败这种免疫反应的能力仍有待了解。布氏细盘菌Leptopilina boulardi和L. heterotoma，两个密切相关的，高感染性的自然寄生性果蝇黑腹果蝇，似乎使用非常不同的感染策略在细胞水平上。在这里，我们进一步表征细胞水平的差异，这两个黄蜂物种的感染特性，使用新衍生的，有毒的近交系，然后使用全基因组微阵列比较果蝇的转录反应。当苍蝇被黑腹类群专家L. boulardi（菌株Lb 17）上调编码蛋白水解酶、Toll和JAK/STAT途径的组分以及黑化级联的许多基因，作为组合的细胞和体液先天免疫应答的一部分，被多面手L.在我们测定的感染后的时间点，异瘤病毒（菌株Lh 14）似乎没有启动免疫转录应答，这可能是由于宿主血细胞（血细胞）的快速毒液介导的裂解。因此，专家寄生蜂似乎在宿主中引起全面的免疫反应，但抑制和/或逃避这种反应的下游成分。鉴于宿主免疫反应的激活可能耗尽宿主的能量资源，专家的感染策略似乎相对不利。然而，我们揭示了通才的高度免疫抑制感染策略的一个潜在的重要健身权衡机制。果蝇（Drosophila melanogaster）已成为研究先天免疫的模型系统，而寄生蜂是果蝇最明显的天然病原体之一，这使其成为研究宿主免疫系统与病原体毒力蛋白之间相互作用的重要系统。我们重点关注了两种密切相关的黄蜂物种：Leptopilina boulardi和L. heterotoma，成功寄生D.黑腹果蝇是自然界的寄主。这两种黄蜂都将载有病毒样颗粒的毒液注射到宿主体内，以防止宿主介导的黑色素包裹和杀死它们的卵。然而，这两种黄蜂的毒液的效果有很大的不同。L.异瘤蛛毒液导致宿主血细胞溶解并阻止宿主产生任何实质性的免疫转录反应，而L.布拉迪毒液对宿主血细胞存活具有相对较弱和局部的作用，并且不阻止免疫应答激活。因此，这些黄蜂使我们能够比较相对免疫抑制与相对免疫逃避寄生虫感染策略在自然系统中的利弊。
Although host–parasitoid interactions are becoming well characterized at the organismal and cellular levels, much remains to be understood of the molecular bases for the host immune response and the parasitoids' ability to defeat this immune response. Leptopilina boulardi and L. heterotoma, two closely related, highly infectious natural parasitoids of Drosophila melanogaster, appear to use very different infection strategies at the cellular level. Here, we further characterize cellular level differences in the infection characteristics of these two wasp species using newly derived, virulent inbred strains, and then use whole genome microarrays to compare the transcriptional response of Drosophila to each. While flies attacked by the melanogaster group specialist L. boulardi (strain Lb17) up-regulate numerous genes encoding proteolytic enzymes, components of the Toll and JAK/STAT pathways, and the melanization cascade as part of a combined cellular and humoral innate immune response, flies attacked by the generalist L. heterotoma (strain Lh14) do not appear to initiate an immune transcriptional response at the time points post-infection we assayed, perhaps due to the rapid venom-mediated lysis of host hemocytes (blood cells). Thus, the specialist parasitoid appears to invoke a full-blown immune response in the host, but suppresses and/or evades downstream components of this response. Given that activation of the host immune response likely depletes the energetic resources of the host, the specialist's infection strategy seems relatively disadvantageous. However, we uncover the mechanism for one potentially important fitness tradeoff of the generalist's highly immune suppressive infection strategy. The fruitfly Drosophila melanogaster has become a model system for the study of innate immunity, and parasitic wasps are one of the most obvious natural pathogens of Drosophila, making this a great system for studying interactions between the host immune system and pathogen virulence proteins. We have focused on two closely related wasp species, Leptopilina boulardi and L. heterotoma, that successfully parasitize D. melanogaster hosts in nature. Both wasps inject venom loaded with virus-like particles into their hosts to prevent host-mediated melanotic encapsulation and killing of their eggs. However, there are substantial differences in the effects of the venom from these two wasp species. L. heterotoma venom causes lysis of host hemocytes (blood cells) and prevents the host from mounting any substantial immune transcriptional response, while L. boulardi venom has a relatively weak and localized effect on host hemocyte survival and does not prevent immune response activation. Thus, these wasps allow us to compare the benefits and drawbacks of relatively immune suppressive versus relatively immune evasive parasite infection strategies in a natural system.
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