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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.
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http://dx.doi.org/10.1038/s41598-020-58375-y | DOI Listing |
Parasite Immunol
September 2025
Department of Parasitology, Leiden University Medical Center, Leiden, the Netherlands.
Schistosome parasites are known to modulate host immune responses, which is achieved in part through the release of excretory/secretory (ES) products, including extracellular vesicles (EVs). During chronic schistosomiasis, increased regulatory responses are found, which include enhanced IL-10 production by B (Breg) cells. ES products from schistosome eggs are able to induce IL-10 production by B cells.
View Article and Find Full Text PDFParasite Immunol
September 2025
Department of Zoology, Panjab University, Chandigarh, India.
Leishmania parasite adeptly evades the host's immune defences by infiltrating macrophages, exploiting apoptotic processes for further dissemination. Among the host's strategies to counter parasitic propagation, the pivotal role of B-cells, specifically B regulatory (Breg) cells, emerges. Recent evidence from in vitro and in vivo studies has thrust Breg cells into the spotlight, attributed to their IL-10 secretion and antigen presentation.
View Article and Find Full Text PDFBiomaterials
September 2025
Institute of Breast Health Medicine, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University and Collaborative Innovation Center, Chengdu, Sichuan, 610041, PR China. Electronic address:
Host immune elimination largely limits the application of oncolytic viruses in clinics. Here, we rationally design a bioactive platelet-based oncolytic adenovirus delivery system. Upon loading adenoviruses, platelets are transformed to a pro-endocytosis status, which facilitates their internalization by circulating tumor cells (CTCs).
View Article and Find Full Text PDFJ Fish Biol
September 2025
College of Animal Science and Technology, Yangzhou University, Yangzhou, China.
Citrobacter freundii, a common zoonotic pathogen affecting humans, livestock and fish, is recognized for its substantial impact on largemouth bass (Micropterus salmoides) mortality. However, the mechanisms of C. freundii infection in largemouth bass remain poorly understood.
View Article and Find Full Text PDFTrends Immunol
September 2025
Baker Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia; Department of Cardiometabolic Health, The University of Melbourne, Melbourne, Victoria 3010, Australia. Electronic address:
Neutrophil extracellular trap (NET) formation, or NETosis, is a key innate immune response that contributes to cardiovascular diseases, including vascular inflammation, atherosclerosis, and thrombosis. In the cardiovascular system, neutrophils encounter mechanical cues such as shear stress, matrix stiffness, and cyclic stretch that influence their activation and NET release. This review examines emerging evidence linking altered mechanotransduction to dysregulated NETosis in vascular aging and cardiovascular pathology.
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