Abstract
Sufficient energy supply to the host immune system is important for resisting pathogens. Therefore, during pathogen infection, the host metabolism is reassigned from storage, growth, and development to the immune system. Previous studies in Drosophila melanogaster have demonstrated that systemic metabolic switching upon an immune challenge is activated by extracellular adenosine signaling, modulating carbohydrate mobilization and redistributing energy to the hemocytes. In the present study, we discovered that symbiotic virus (SmBV) of the parasitoid wasp Snellenius manilae is able to down-regulate the extracellular adenosine of its host, Spodoptera litura, to inhibit metabolism switching. The decreased carbohydrate mobilization, glycogenolysis, and ATP synthesis upon infection results in the host being unable to supply energy to its immune system, thus benefitting the development of wasp larvae. When we added adenosine to the infected S. litura larvae, we observed enhanced host immune responses that decreased the pupation rate of S. manilae. Previous studies showed that after pathogen infection, the host activates its adenosine pathway to trigger immune responses. However, our results suggest a different model: we found that in S. manilae, SmBV modulates the host adenosine pathway such that wasp eggs and larvae can evade the host immune response.
Highlights
Sufficient energy supply to the host immune system is important for resisting pathogens
Results showed that the hemocytes collected from symbiotic virus (SmBV)-infected larvae exhibited decreased phagocytic activity compared with the control, indicating attenuated cellular immunity after SmBV infection (Fig. 1A)
Phagocytosis quantitation results showed that only 19% of the hemocytes from SmBV-infected larvae phagocytized FITC-labeled E. coli in comparison to 32% of non-infected larvae and 40% of AcMNPV-infected larvae (Fig. 1B)
Summary
Sufficient energy supply to the host immune system is important for resisting pathogens. Previous studies in Drosophila melanogaster have demonstrated that systemic metabolic switching upon an immune challenge is activated by extracellular adenosine signaling, modulating carbohydrate mobilization and redistributing energy to the hemocytes. When vertebrates are infected by pathogens, host immune responses are activated, which are intimately associated with metabolic switching including the redistribution of energy supply and increased glycolysis and glucose consumption in the immune system[1,2]. This metabolic reprogramming has been observed in Drosophila, whereby delayed development and increased carbohydrate mobilization (hyperglycemia) was found after infection with parasitoid wasps or bacteria[3,4]. Previous studies showed increased adenosine and circulative glucose levels after pathogen entry activate immune responses, whereas our study shows different results: after insects are infected by SmBVs, adenosine, glucose, glycogenolysis and ATP synthesis are attenuated, resulting in a loss of immune responses
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