Mortality effects of eicosanoid biosynthesis inhibitors on Spodoptera littoralis larvae co-injected with the bacteria, Serratia marcescens

The first step of the cellular defense reactions to bacterial, fungal and some viral infections in insects is nodulation. We posed the hypothesis that Spodoptera littoralis, expresses melanoic nodulation reactions to bacterial challenge and that injecting S. littoralis larvae with eicosanoid biosnthesis inhibitors (EBIs) plus bacteria would increase larval mortality. Injecting larvae with EBIs, immediately before intrahemocoelic injections of the bacterium, Serratia marcescens, sharply reduced the nodulation response to bacterial challenges. Separate treatments with specific inhibitors including dexamethasone (a phospholipase A(2) inhibitor), indomethacin, naproxen, ibuprofen, (cyclooxygenase inhibitors), esculetin (a lipoxygenase inhibitor) and Phenidone (dual cyclooxgenase/lipoxygenase inhibitor) impaired the ability of S. littoralis to form nodules in reaction to bacterial challenge. All concentrations of S. marcescens alone, applied to S. littoralis, caused low mortality of the larvae. However, an increased mortality of the larvae was seen when S. marcescens was co-injected with the EBIs with different modes of action. These findings support our hypothesis that virulent effects of entomopathogenic bacteria can be increased when S. littoralis immune systems were suppressed.