In insect midgut, prostaglandins (PGs) play a crucial role in defending bacterial and malarial pathogens. However, little is known about the PG signalling pathway in the midgut. A dual oxidase (Se-Duox) with presumed function of catalysing reactive oxygen species (ROS) production in the midgut was identified in beet armyworm, Spodoptera exigua. Se-Duox was expressed in all developmental stages, exhibiting relatively high expression levels in the midgut of late larval instars. Se-Duox expression was upregulated upon bacterial challenge. RNA interference (RNAi) of Se-Duox expression significantly suppressed ROS levels in the midgut lumen. The suppression of ROS levels increased insecticidal activity of Serratia marcescens after oral infection. Interestingly, treatment with a PLA₂ inhibitor prevented the induction of Se-Duox expression in response to bacterial challenge. On the other hand, addition of its catalytic product rescued the induction of Se-Duox expression. Especially, PG synthesis inhibitor significantly suppressed Se-Duox expression, while the addition of PGE₂ or PGD₂ rescued the inhibition. Subsequent PG signals involved cAMP and downstream components because specific inhibitors of cAMP signal components such as adenylate cyclase (AC) and protein kinase A (PKA) significantly inhibited Se-Duox expression. Indeed, addition of a cAMP analogue stimulated Se-Duox expression in the midgut. Furthermore, individual RNAi specific to PGE₂ receptor (a trimeric G-protein subunit), AC, PKA or cAMP-responsive element-binding protein resulted in suppression of Se-Duox expression. These results suggest that PGs can activate midgut immunity via cAMP signalling pathway by inducing Se-Duox expression along with increased ROS levels.

在昆虫中肠中，前列腺素 (PG) 在防御细菌和疟疾病原体方面起着至关重要的作用。然而，对中肠中的 PG 信号通路知之甚少。在甜菜夜蛾Spodoptera exigua中鉴定出一种双重氧化酶 ( Se-Duox )，推测其具有催化中肠中活性氧 (ROS) 产生的功能。Se-Duox在所有发育阶段均有表达，在幼虫后期的中肠中表现出相对较高的表达水平。Se-Duox表达在细菌攻击后上调。Se-Duox表达的RNA 干扰 (RNAi)显着抑制了中肠腔中的 ROS 水平。ROS水平的抑制增加了杀虫活性口腔感染后粘质沙雷菌。有趣的是，用 PLA ₂抑制剂处理阻止了Se-Duox表达的诱导以响应细菌攻击。另一方面，添加其催化产物挽救了Se-Duox表达的诱导。特别是PG合成抑制剂显着抑制Se-Duox的表达，而PGE ₂或PGD _{2 的加入则}解除了抑制。随后的 PG 信号涉及 cAMP 和下游成分，因为 cAMP 信号成分的特异性抑制剂如腺苷酸环化酶 (AC) 和蛋白激酶 A (PKA) 显着抑制Se-Duox表达。事实上，添加 cAMP 类似物刺激了中肠中的Se-Duox表达。此外，对 PGE ₂受体（三聚体 G 蛋白亚基）、AC、PKA 或 cAMP 响应元件结合蛋白具有特异性的个体 RNAi导致Se-Duox表达的抑制。这些结果表明 PGs 可以通过 cAMP 信号通路通过诱导Se-Duox表达以及增加 ROS 水平来激活中肠免疫。