Toll recognition signal activates oenocytoid cell lysis via a crosstalk between plasmatocyte-spreading peptide and eicosanoids in response to a fungal infection.

Plasmatocyte-spreading peptide (PSP) activates hemocyte-spreading behavior in response to various microbial pathogens. Its homolog, growth-blocking peptide, has several functions that activate immune cells and induce oenocytoid cell lysis (OCL). OCL is required for release of prophenoloxidase from oenocytoids in the beet armyworm, Spodoptera exigua. Injection of PSP to S. exigua larvae significantly induced in vivo OCL and resulted in significant increase of phenoloxidase (PO) activity. A fungal infection induced PSP expression and also significantly increased OCL. RNA interference (RNAi) of PSP expression significantly suppressed OCL induction and subsequently inhibited PO activation. Interestingly, an addition of dexamethasone (a specific phospholipase A₂ inhibitor) inhibited the PSP activity to induce OCL. Toll signal pathway was associated with PSP action on inducing OCL because RNAi of Toll expression suppressed PSP expression and subsequent OCL induction. However, an addition of PSP to the larvae under RNAi of Toll expression rescued the progress of OCL.