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Endocrine Mediation of Insect Immunity
Insects have a highly efficient innate immunity consisting of cellular and humoral responses. Upon microbial pathogen infection, pattern recognition receptors specifically recognize pathogen types and trigger the programmed immune responses via immune mediators, such as cytokine, biogenic monoamines, and eicosanoids. In addition to these canonical immune mediators, two insect developmental hormones of juvenile hormone (JH) and 20-hydroxyecdysone (20E) also modulate immune responses. JH suppresses a cellular immune response, while 20E antagonizes the JH action. In Tribolium castaneum, JH mediates cellular immune responses via non-nuclear receptor(s). When Met (the JH nuclear receptor) expression was silenced by its specific double-stranded RNA, T. castaneum underwent precocious metamorphosis. Under these RNA interference (RNAi) conditions, JH still mediates the cellular immune responses. The addition of calphostin C (a PKC inhibitor) or ouabain (a Na + -K + ATPase inhibitor) significantly suppressed the JH mediation on the cellular immune responses, suggesting the presence of a novel JH receptor(s) at nonnuclear regions.
Eicosanoids are a group of oxygenated C20 polyunsaturated fatty acids. They mediate various insect physiological processes including reproduction, excretion, and immunity. Arachidonic acid (AA) is a main precursor of eicosanoid biosynthesis. Phospholipase A2 (PLA2) catalyzes AA release from phospholipids. Subsequent oxygenases of cyclooxygenase (COX) or lipoxygenase (LOX) transform AA to prostaglandins (PGs) or leukotrienes (LTs). In a model insect, Spodoptera exigua, both PGs and LTs mediate both cellular and humoral immune responses. In addition to the physiological significance of the secretory PLA2 (sPLA2), a recent genome analysis identified a novel cellular PLA2 (cPLA2) in S. exigua, which mediates the immune responses. Especially, eicosanoids mediate prophenoloxidase (PPO) activation by stimulating release of PPO from oenocytoid hemocytes. A G protein-coupled receptor is identified in oenocytoids and highly specific to PGE2. Subsequent calcium and PKC pathways mediate PG signal to activate a specific ion channel, Na + -K + -Cl - -cotransporter (NKCC), which generates an osmotic shock to induce cell lysis of oenocytoids to release internal PPO. The released PPO would be activated by a cascade of serine proteases and involved in various immune responses. Eicosanoids also mediate antimicrobial peptide gene expression in response to the bacterial infection. Lack of eicosanid biosynthesis results in a significant immunosuppression. This kind of immunosuppression is exploited by an entomopathogenic bacterium, Xenorhabdus nematophila, to proliferate in the infected larvae without adverse attack to the bacteria by host immune defense. Eight PLA2 inhibitors have been chemically identified and used to develop novel biopesticides. Even though several chemical analyses using various insect systems indicate PG and LT eicosanoids, COX and LOX genes are not identified. Furthermore, little information is available in PG receptors in insects. Thus, signal transduction of eicosanoids in insects remains unresolved. Eicosanoid biosynthesis and signal transduction need to be explored to understand the significant roles of eicosanoids in insect physiological processes.
