Prostaglandin mediates down-regulation of phenoloxidase activation of Spodoptera exigua via plasmatocyte-spreading peptide-binding protein.

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.