Eicosanoid‐induced calcium signaling mediates cellular immune responses of Tenebrio molitor

Abstract

AbstractCalcium signaling is associated with actin cytoskeleton rearrangement. It is required for expressing cellular immune responses of insect hemocytes. Eicosanoids mediate immune responses by cytoskeleton rearrangement against various pathogen infections in insects. The objective of this study was to investigate cellular immune responses of a mealworm, Tenebrio molitor L. (Coleoptera: Tenebrionidae). The hypothesis tested was that immune responses would be mediated by calcium signaling associated with eicosanoid mediation. Larvae of T. molitor possessed at least four morphological types of hemocytes, most (almost 75%) of which were granulocytes and plasmatocytes. They all exhibited a hemocyte‐spreading behavior by F‐actin extension. Upon bacterial infection, hemocytes exhibited phagocytosis and formed hemocytic nodules. Intracellular calcium was detected in hemocytes. Its amount increased with increasing incubation time after bacterial infection. Inhibition of calcium influx or release from endoplasmic reticulum using specific inhibitors prevented cellular immune responses. Interestingly, treatment with an eicosanoid biosynthesis inhibitor suppressed calcium signals induced by bacterial challenge. Furthermore, treatment with naproxen, a prostaglandin (PG) synthesis inhibitor, or esculetin, a leukotriene synthesis inhibitor, also inhibited the increase of calcium concentration in hemocytes. Among eicosanoids, PGE2 highly stimulated the increase of calcium signals. These results suggest that cellular immune responses of T. molitor are triggered by calcium signaling, which is up‐regulated by eicosanoids.