The eicosanoid signaling pathway mediates insect immune reactions to a wide range of stimuli. This pathway begins with the biosynthesis of arachidonic acid (AA) from the hydrolysis of phospholipids catalyzed by phospholipase A 2 (PLA 2 ). We report here that the PLA 2 inhibitor, dexamethasone (DEX), impaired the innate immune response including nodulation, encapsulation, and melanization in Ostrinia furnacalis larvae, while AA partially reversed these effects of DEX. We cloned a full-length complementary DNA encoding a PLA 2 , designated as OfsPLA 2 , from O. furnacalis. The open reading frame of OfsPLA 2 encodes a 195-amino acid residue protein with a 22-residue signal peptide. Sequence alignment analyses indicated that O. furnacalis PLA 2 might be a Group III secretory PLA 2 . The highest transcript levels of OfsPLA 2 were detected in the fat body, and its transcript levels increased dramatically after infection with Escherichia coli, Micrococcus luteus, or Beauveria bassiana. Recombinant OfsPLA 2 significantly induced prophenoloxidase (PPO) activation in larval hemolymph in the presence of Ca 2+ and encapsulation of agarose beads. Injection of recombinant OfsPLA 2 into larvae resulted in increased transcript levels of attacin, defencin, and moricin-3 genes. Our results demonstrate the involvement of the eicosanoid signaling pathway in the innate immune response of O. furnacalis larvae and provide new information about the roles of O. furnacalis secretory PLA 2 in activating PPO and antimicrobial peptide production.