Toll/IMD signal pathways mediate cellular immune responses via induction of intracellular PLA ₂ expression

Phospholipase A₂ (PLA₂ ) hydrolyzes fatty acids from phospholipids at the sn-2 position. Two intracellular PLA₂ s, iPLA₂ A and iPLA₂ B, have been found in Spodoptera exigua. Both are calcium-independent cellular PLA₂ . Their orthologs have been found in other insects. These two iPLA₂ s are different in ankyrin motif of N terminal region. The objective of this study was to determine whether Toll/immune deficiency (IMD) signal pathways could mediate cellular immune responses via induction of iPLA₂ expression. Both iPLA ₂ s were expressed in all developmental stages of S. exigua, showing the highest expression in the adult stage. During larval stage, hemocyte is the main tissue showing expression of these iPLA₂ s. Both iPLA₂ s exhibited similar expression patterns after immune challenge with different microbial pathogens such as virus, bacteria, and fungi. Promoter component analysis of orthologs encoded in S. frugiperda indicated nuclear factor-κB- and Relish-responsible elements on their promoters, suggesting their expression in S. exigua under Toll/IMD immune signaling pathways. RNA interference (RNAi) of MyD88 or Pelle under Toll pathway suppressed inducible expression levels of both iPLA₂ s in response to Gram-positive bacteria containing Lys-type peptidoglycan or fungal infection. In contrast, RNAi against Relish under IMD pathway suppressed both iPLA₂ s in response to infection with Gram-negative bacteria. Under RNAi conditions, hemocytes significantly lost cellular immune response measured by nodule formation. However, addition of arachidonic acid (a catalytic product of PLA₂ ) rescued such immunosuppression. These results suggest that Toll/IMD signal pathways can mediate cellular immune responses via eicosanoid signaling by inducing iPLA₂ expression.