Department of Bioresource Sciences, Andong National University, Andong, Republic of Korea.
Arch Insect Biochem Physiol. 2014 Apr;85(4):234-47. doi: 10.1002/arch.21156. Epub 2014 Feb 24.
Insect immunity is innate and highly efficient to defend against various pathogens. However, uncontrolled excessive immune responses would be highly detrimental and energy-consuming processes. An insect cytokine, plasmatocyte-spreading peptide (SePSP), induces hemocyte-spreading behavior as well as activates phenoloxidase (PO) in the beet armyworm, Spodoptera exigua. A hemocyte transcriptome of S. exigua contains a partial sequence of a putative PSP-binding protein (SePSP-BP1). SePSP-BP1 was expressed in most larval stages except in the last instar. However, a bacterial challenge induced SePSP-BP1 expression in the last instar especially in hemocytes and fat body. Injecting a double-stranded RNA specific to SePSP-BP1 (dsPSP-BP1) suppressed the induction of SePSP-BP1 expression in response to bacterial challenge. The larvae treated with dsPSP-BP1 suffered high mortality to infection of nonpathogenic bacteria due to uncontrolled high PO activity. SePSP significantly induced PO activity. The eicosanoid synthesis inhibitor, dexamethasone (DEX), inhibited SePSP-mediated PO activation. However, treatment with prostaglandin E2 (PGE2) induced a transient increase of PO activity under DEX treatment. Treatment of dsPSP decreased the duration of PO activation induced by PGE2, while treatment of dsPSP-BP1 increased the induced period. These results suggest that prostaglandin mediates PSP signals in both upregulation of PO activity and its subsequent downregulation via SePSP-BP1.
昆虫的先天免疫系统高效且能抵御多种病原体，但过度的免疫反应会对昆虫造成严重的损害并消耗大量的能量。昆虫细胞因子浆细胞扩展肽（SePSP）可诱导血淋巴细胞扩展行为，并激活甜菜夜蛾（Spodoptera exigua）的酚氧化酶（PO）。甜菜夜蛾血细胞转录组中包含一个假定的 PSP 结合蛋白（SePSP-BP1）的部分序列。SePSP-BP1 在幼虫的大多数阶段都有表达，除了最后一龄。然而，细菌挑战会诱导 SePSP-BP1 在最后一龄，特别是在血淋巴细胞和脂肪体中表达。注射针对 SePSP-BP1 的双链 RNA（dsPSP-BP1）可抑制细菌挑战诱导的 SePSP-BP1 表达。用 dsPSP-BP1 处理的幼虫因 PO 活性失控而遭受高死亡率，从而感染非致病性细菌。SePSP 可显著诱导 PO 活性。类二十烷酸合成抑制剂地塞米松（DEX）抑制了 SePSP 介导的 PO 激活。然而，在 DEX 处理下，前列腺素 E2（PGE2）处理会诱导 PO 活性短暂增加。dsPSP 处理会缩短 PGE2 诱导的 PO 活性激活时间，而 dsPSP-BP1 处理会增加诱导时间。这些结果表明，前列腺素通过 SePSP-BP1 介导 PSP 信号，在 PO 活性的上调及其随后的下调中发挥作用。
