A nuclear receptor, Met, mediates juvenile hormone (JH) action to control gene expressions associated with metamorphosis in many insects. In this study, we showed that RNA interference (RNAi) of the Met or Kruffel homolog 1 (Kr-h1) induced the precocious metamorphosis of Tribolium castaneum larvae. JH significantly inhibited cellular immune response of T. castaneum hemocyte by suppressing hemocyte-spreading behaviour and nodule formation in response to bacterial injection. However, either RNAi of Met or Kr-h1 expression did not prevent the JH-inhibitory effect on hemocyte behaviors. However, several inhibitors specific to JH membrane action significantly inhibit the JH action hemocytes. These results suggest that JH responsiveness of hemocyte is not mediated by the nuclear receptor.

Insect blood cells, hemocytes, inhibit spreading behavior upon bacterial challenge to perform cellular immune responses. Hemocyte spreading is accomplished by cytoskeleton rearrangement, which is activated by various immune mediators, such as biogenic monoamins, plasmatocyte-spreading peptide(psp), and eicosanoids. However, little is known how these, immune mediators. acitvate hemocyte spreading behavior. A small G protein, Rac1, gene was identified in hemocytes of Spodoptera exiqua. Its expressed in most developmental stages accept egg and expecially expresses in hemocytes and fat body of Larval stage. In response to bacterial challenge, its expression was segnificantly up-regulated. However, RNA inteference (RNAi) of Rac1 expression inhibited hemocyte spreading behavior. under RNAi condition of Rac1, octopamine and psp failed to activate hemocyte spreading behavior. Interestingly, as addition of prostaglandinE2 to the RNAiconditioned Larval rescued the mediation of octopamine and psp. These results indicate that Rac1 is required for mediation of octopamine and psp on hemocytespreading behavior and suggest that Rac1 may activate eicosanoid biosnthesis.

Two entomopathogenic bacteria, Xenorhadus nematophila and Photorhabdus temperata temperata, are known to suppress immune responses of target insects by inhibiting eicosanoid biosynthesis. This study analyzed these bacterial metabolites in their effects on hemocyte-spreading behavior of the beet armyworm, Spodoptera exigua. Both bacterial culture broth significantly inhibited the hemocyte-spreading behavior, at which the culture broth derived from the stationary growth phase had the most potent effect. Three identified eicosanoid synthesis inhibitors (benzylideneacetone, PY and Ac-FGV) impaired the hemocyte-spreading behavior of S. xigua, at which benzylideneacetone was the most potent. These three compounds share a common chemical structure: a pentenebenzene ring. Alternation of this common structure resulted in significant loss of their inhibitory activity to the hemocyte-spreading behavior.