Symbiotic microbes play a crucial role in regulating parasite–host interactions; however, the role of bacterial associates in parasite–host interactions requires elucidation. In this study, we showed that, instead of introducing numerous symbiotic bacteria, dispersal of 4th-stage juvenile (J_IV) pinewood nematodes (PWNs), Bursaphelenchus xylophilus, only introduced few bacteria to its vector beetle, Monochamus alternatus (Ma). J_IV showed weak binding ability to five dominant bacteria species isolated from the beetles’ pupal chamber. This was especially the case for binding to the opportunistic pathogenic species Serratia marcescens; the nematodes’ bacteria binding ability at this critical stage when it infiltrates Ma for dispersal was much weaker compared with Caenorhabditis elegans, Diplogasteroides asiaticus, and propagative-stage PWN. The associated bacterium S. marcescens, which was isolated from the beetles’ pupal chambers, was unfavorable to Ma, because it caused a higher mortality rate upon injection into tracheae. In addition, S. marcescens in the tracheae caused more immune effector disorders compared with PWN alone. Ma_Galectin2 (MaGal2), a pattern-recognition receptor, was up-regulated following PWN loading. Recombinant MaGal2 protein formed aggregates with five dominant associated bacteria in vitro. Moreover, MaGal2 knockdown beetles had up-regulated prophenoloxidase gene expression, increased phenoloxidase activity, and decreased PWN loading. Our study revealed a previously unknown strategy for immune evasion of this plant pathogen inside its vector, and provides novel insights into the role of bacteria in parasite–host interactions.

中文翻译：

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由 MaGal2 诱导的一种新的无细菌策略促进松木线虫逃避其载体甲虫的免疫反应

共生微生物在调节寄生虫-宿主相互作用中起着至关重要的作用；然而，细菌关联物在寄生虫-宿主相互作用中的作用需要阐明。在这项研究中，我们表明，不是引入大量共生细菌，而是散布第 4 阶段幼年 (J _IV ) 松材线虫 (PWNs)，松材线虫，仅将很少的细菌引入其载体甲虫Monochamus alternatus ( Ma )。J _IV对从甲虫的蛹室中分离出来的五种优势细菌种类显示出较弱的结合能力。与机会致病菌Serratia marcescens结合的情况尤其如此; 线虫在渗入Ma进行传播的这个关键阶段的细菌结合能力与秀丽隐杆线虫、Diplogasteroides asiaticus和繁殖期 PWN相比要弱得多。从甲虫的蛹室中分离出的相关细菌S. marcescens对Ma不利，因为它在注射到气管时会导致更高的死亡率。此外，与单独的 PWN 相比，气管中的粘质沙门氏菌引起更多的免疫效应障碍。Ma_Galectin2 (MaGal2) 是一种模式识别受体，在加载 PWN 后上调。重组 MaGal2 蛋白与五种优势相关细菌形成聚集体体外。此外，MaGal2 敲除甲虫具有上调酚氧化酶原基因表达、酚氧化酶活性增加和 PWN 负载降低。我们的研究揭示了一种以前未知的在其载体内逃避这种植物病原体的免疫策略，并为细菌在寄生虫-宿主相互作用中的作用提供了新的见解。