摘要
Nodulation is the predominant cellular defense reaction to bacterial challenges in insects. In this study, third instar larvae of Chrysomya megacephala were injected with bacteria, Escherichia coli K 12 （10^6 CFU/mL, 2μL）, immediately prior to injection of inhibitors of eicosanoid biosynthesis, which sharply reduced nodulation response. Test larvae were treated with specific inhibitors ofphospholipase A2 （dexamethasone）, cyclo- oxygenase （indomethacin, ibuprofen and piroxicam）, dual cyclo-oxygenase/lipoxygenase （phenidone） and lipoxygenase （esculetin） and these reduced nodulation except esculetin. The influence of bacteria was obvious within 2 h of injection （5 nodules/larva）, and increased to a maximum after 8 h （with 15 nodules/larva）, and then significantly reduced over 24 h （9 nodules/larva）. The inhibitory influence of dexamethasone was apparent within 2 h of injection （4 vs. 5 nodules/larva）, and nodulation was significantly reduced, compared to control, over 24 h （5 vs. 8 nodules/larva）. Increased dosages of ibuprofen, indomethacin, piroxicam and phenidone led to decreased numbers of nodules. Nodules continued to exist during the pupal stage. However, the effects of dexamethasone were reversed by treating bacteria-injected insects with an eicosanoid-precursor polyunsaturated fatty acid, arachidonic acid. These findings approved our view that eicosanoid can mediate cellular defense mechanisms in response to bacterial infections in another Dipteran insect C. rnegacephala.
Nodulation is the predominant cellular defense reaction to bacterial challenges in insects. In this study, third instar larvae of Chrysomya megacephala were injected with bacteria, Escherichia coli K 12 （10^6 CFU/mL, 2μL）, immediately prior to injection of inhibitors of eicosanoid biosynthesis, which sharply reduced nodulation response. Test larvae were treated with specific inhibitors ofphospholipase A2 （dexamethasone）, cyclo- oxygenase （indomethacin, ibuprofen and piroxicam）, dual cyclo-oxygenase/lipoxygenase （phenidone） and lipoxygenase （esculetin） and these reduced nodulation except esculetin. The influence of bacteria was obvious within 2 h of injection （5 nodules/larva）, and increased to a maximum after 8 h （with 15 nodules/larva）, and then significantly reduced over 24 h （9 nodules/larva）. The inhibitory influence of dexamethasone was apparent within 2 h of injection （4 vs. 5 nodules/larva）, and nodulation was significantly reduced, compared to control, over 24 h （5 vs. 8 nodules/larva）. Increased dosages of ibuprofen, indomethacin, piroxicam and phenidone led to decreased numbers of nodules. Nodules continued to exist during the pupal stage. However, the effects of dexamethasone were reversed by treating bacteria-injected insects with an eicosanoid-precursor polyunsaturated fatty acid, arachidonic acid. These findings approved our view that eicosanoid can mediate cellular defense mechanisms in response to bacterial infections in another Dipteran insect C. rnegacephala.
