Immune defense is indispensible for insect survival. However, uncontrolled and excessive immune responses would be highly detrimental and energy-consuming processes. An insect cytokine, plasmatocyte-spreading peptide (PSP), induces hemocyte-spreading behavior as well as activating 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-BP). SePSP-BP was expressed in all developmental stages especially in hemocytes and fat body. A quantitative RT-PCR showed that the bacterial infection significantly up-regulated the expression level of SePSP-BP. A double-stranded RNA specific to SePSP-BP (dsRNASePSP-BP) was injected and suppressed SePSP-BP expression even in response to bacterial challenge. The larvae treated with dsRNASePSP-BPsuffered high mortality to infection of nonpathogenic bacteria and prolonged high PO activity after the immune challenge. These results suggest that SePSP-BP may play a role in suppressing immune responses as a negative controller

Insect blood cells (hemocytes) play a key role in defense against parasites and other pathogenic organisms that infect insects. Cellular immune responses exhibited by hemocytes are acute and effective to initially suppress pathogenic processes. Subsequently humoral immune responses executed by antimicrobial peptides completely cleared the pathogens with help of hemocytes. Two immune mediators, plasmatocyte-spreading peptide (PSP) and eicosanoid, are known to mediate cellular immune responses by activating hemocyte behavior. This study was focused on how these two immune mediators work together to express hemocyte spreading behavior. Both PSP and prostaglandins stimulate hemocyte spreading in dose-dependent manners in the beet armyworm, Spodoptera exigua. Interstingly, inhibition of eicosanoid biosynthesis inhibited PSP activity on mediating the hemocyte-spreading behavior. However, the addition of eicosanoid biosynthesis precursor, arachidonic acid, rescued the hemocytespreading activity. Inhibition of PSP or its receptor by each RNA interference are now under investigation to test whether PSP triggers eicosanoid signaling. These results suggest that there is a cross-talk between PSP and eicosanoid to express hemocyte-spreading behavior in response to bacterial challenge