Eicosanoids Mediate Nodulation Responses to Bacterial Infections in Larvae

Nodulation is the temporally and quantitatively predominant cellular defense response to bacterial infection in insects and other invertebrates. Inhibition of eicosanoid biosynthesis in larvae of the tenebrionid beetle, Zophobas atratus, immediately prior to intrahemocoelic injections with heat killed preparations of the bacterium, Serratia marcescens, strongly reduced the nodulation response. Separate treatments with specific inhibitors of phospholipase A,, cyclooxygenase, and lipoxygenase reduced nodulation, supporting the view that nodule formation is a complex process involving both cyclooxygenase and lipoxygenase products. The inhibitory effects of the phospholipase A, inhibitor, dexamethasone, on nodulation were apparent 1 h after infection, and the effects increased, relative to controls, over 24 h. The dexamethasone effects were expressed in a dose-dependent manner, and they were reversed by treating bacteria injected insects with the eicosanoid-precursor polyunsaturated fatty acid, arachidonic acid (C20:4n-6). Treatments with the saturated fatty acid, 16:0, which is not an eicosanoid precursor, did not reverse the dexamethasone effects on nodulation. The insects contain low levels of three eicosanoid precursor polyunsaturated fatty acids in six different tissues, and fat body preparations are competent to produce both cyclooxygenase and lipoxygenase products. These findings strongly support the identification of nodulation as a specific insect cellular defense mechanism that is mediated by eicosanoids.