The prophenoloxidase system in Drosophila participates in the anti-nematode immune response
The prophenoloxidase system in Drosophila participates in the anti-nematode immune response
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DOI：
10.1016/j.molimm.2019.03.008
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发表时间：
2019-05-01
影响因子：
3.6
通讯作者：
Eleftherianos, Ioannis
中科院分区：
文献类型：
--
作者：
Cooper, Dustin;Wuebbolt, Caitlin;Eleftherianos, Ioannis
黑腹果蝇依靠进化上保守的先天免疫系统来保护自己免受潜在致命病原体的侵害。损伤或感染后最早激活的途径之一是黑化途径，其负责在损伤部位或入侵微生物上合成和沉积黑色素。三个基因，PPO 1 -3，编码酚氧化酶原（PPO），酚氧化酶（PO）的非活性前体，是负责黑色素的产生后，通过免疫激发激活。一种能够感染D.黑腹线虫是昆虫病原线虫。斯氏线虫与嗜热小杆菌之间存在着互惠关系，是一种重要的生物防治剂。线虫-细菌复合体（共生线虫）可以分离，产生“纯”线虫，没有它们的相关细菌，它们仍然能够感染和杀死D。黑腹果蝇为了研究D.黑腹菌黑化途径参与抗线虫免疫应答，共生和纯生S. carpocapsae为研究材料。黑腹果蝇存活、PPO基因表达和PPO活化成PO。我们的研究表明，所有三个D。黑腹线虫PPO基因有助于存活，然而，在无菌或共生线虫感染期间，似乎只有PPO 1或PPO 3上调。此外，我们目前的数据表明，一个复杂的监管系统之间存在的PPO，可能允许补偿的PPO的。此外，我们发现，无菌线虫感染导致更高水平的PO，这表明X。嗜热菌抑制这种激活。我们还首次报道了板层细胞的分化，板层细胞是D. melanogaster对共生菌S.果荚线虫感染。我们的研究结果表明黑化途径在线虫感染的应答中起着重要的作用，并证明了这种应答是如何被S。果荚线虫及其共生X.嗜热菌。
Drosophila melanogaster relies on an evolutionarily conserved innate immune system to protect itself from potentially deadly pathogens. One of the earliest pathways activated after injury or infection is the melanization pathway, which is responsible for synthesizing and depositing melanin at the site of injury, or onto invading microbes. Three genes, PPO1-3, encoding prophenoloxidase (PPO), an inactive precursor of phenoloxidase (PO), are responsible for the production of melanin after their activation via immune challenge. One pathogen capable of infecting D. melanogaster are entomopathogenic nematodes. Steinernema carpocapsae nematodes exist in a mutualistic relationship with Xenorhabdus nematophila bacteria and are an important biological control agent for controlling insect pests. The nematode-bacteria complex (symbiotic nematodes) can be separated, creating "axenic" nematodes, devoid of their associated bacteria, which are still capable of infecting and killing D. melanogaster. In order to investigate how the D. melanogaster melanization pathway contributes to the anti nematode immune response, symbiotic and axenic S. carpocapsae were used to study D. melanogaster survival, PPO gene expression, and activation of PPO to PO. Our research suggests that the expression of all three D. melanogaster PPO genes contributes to survival, however only PPO1 or PPO3 appear to be up-regulated during axenic or symbiotic nematode infection. Additionally, we present data suggesting that a complex regulatory system exists between PPOs, potentially allowing for the compensation of PPOs by one another. Further, we found that axenic nematode infection leads to higher levels of PO, suggesting that X. nematophila suppresses this activation. We also report for the first time the differentiation of lamellocytes, a specialized type of hemocytes in D. melanogaster, in response to symbiotic S. carpocapsae nematode infection. Our results suggest an important role played by the melanization pathway in response to nematode infection, and demonstrate how this response can be manipulated by S. carpocapsae nematodes and their mutualistic X. nematophila bacteria.