Abstract
Background: The larval stages of Echinococcus granulosus sensu lato (E. granulosus s.l) infection can alter B cell function and affect host anti-infective immunity, but the underlying mechanism remains unclear. The newly emerging immunometabolism highlights that several metabolites are key factors in determining the fate of immune cells, which provides a new insight for exploring how larval E. granulosus s.l. infection remodels B cell function. This study investigated the metabolomic profiles of B cells in mice infected with E. granulosus s.l. protoscoleces (PSC).Results:Total CD19+ B cells, purified from the spleen of infected mice, showed significantly increased production of IL-6, TNF-α, and IL-10 after exposure to LPS in vitro. Moreover, the mRNA expression of metabolism related enzymes in B cells was remarkably disordered post infection. In addition, differential metabolites were identified in B cells after infection. There were 340 differential metabolites (83 upregulated and 257 downregulated metabolites) identified in the positive ion model, and 216 differential metabolites (97 upregulated and 119 downregulated metabolites) identified in the negative ion mode. Among these, 64 differential metabolites were annotated and involved in 68 metabolic pathways, including thyroid hormone synthesis, the metabolic processes of glutathione, fructose, mannose, and glycerophospholipid. Furthermore, several differential metabolites such as glutathione, taurine, and inosine were validated to regulate the cytokine production in LPS stimulated B cells.Conclusion:Infection with the larval E. granulosus s.l. causes metabolic reprogramming in the intrinsic B cells of mice, which provides the first evidence for understanding the role and mechanism of B cells in parasite anti-infective immunity from the viewpoint of immunometabolism.
Highlights
Cystic echinococcosis (CE) is a zoonosis caused by the larval stages of Echinococcus granulosus sensu lato (E. granulosus s.l.) and is one of the neglected tropical diseases recognized by the World Health Organization [1, 2]
Our previous studies have shown that EgPSC infection or its derived ESPs can elevate IL-10 production in splenic B cells and increase the percentage of Bregs in vivo and in vitro, respectively [11, 18]
To further explore the effects of secondary CE infection on B cell function, splenic CD19+B cells were sorted from control and infected mice and cultured with a vehicle or LPS (10 μg/ml) for 24 h
Summary
Cystic echinococcosis (CE) is a zoonosis caused by the larval stages of Echinococcus granulosus sensu lato (E. granulosus s.l.) and is one of the neglected tropical diseases recognized by the World Health Organization [1, 2]. Understanding the molecular mechanism of these strategies is beneficial for identifying the host-parasite interplay and developing novel immunologic intervention strategies for preventing and controlling CE. The larval stages of Echinococcus granulosus sensu lato (E. granulosus s.l) infection can alter B cell function and affect host anti-infective immunity, but the underlying mechanism remains unclear. The newly emerging immunometabolism highlights that several metabolites are key factors in determining the fate of immune cells, which provides a new insight for exploring how larval E. granulosus s.l. infection remodels B cell function. This study investigated the metabolomic profiles of B cells in mice infected with E. granulosus s.l. protoscoleces (PSC)
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