Background: Alveolar Echinococcosis (AE) is a zoonotic parasitic disease caused by Echinococcus multilocularis, but its pathogenesis remains unclear. The primary objective of this study is to explore whether Echinococcus multilocularis protoscoleces (PSCs) regulate macrophage polarization and glucose metabolism by PI3K/Akt/mTOR signaling pathway.Methods: Macrophage polarization were analyzed by ow cytometry, PI3K, Akt, pAKT, and mTOR were detected by western blot, and cell metabolic was analyzed by seahorse.Results: Large numbers of CD68 + macrophages gathered in close liver issue from the lesion in AE patients. PSCs preferentially differentiated into M2 macrophages and the expressions of HK1, PFKL, PKM2, PI3K, pAKT, and mTOR increased with the extension of co-culture time.Conclusions: Echinococcus multilocularis protoscoleces enhance glycolysis to promote M2 macrophages through PI3K/Akt/mTOR signaling pathway.

Background: Alveolar Echinococcosis (AE) is a zoonotic parasitic disease caused by Echinococcus multilocularis, but its pathogenesis remains unclear. The primary objective of this study is to explore whether Echinococcus multilocularis protoscoleces (PSCs) regulate macrophage polarization and glucose metabolism by PI3K/Akt/mTOR signaling pathway.Methods: Macrophage polarization were analyzed by flow cytometry, PI3K, Akt, pAKT, and mTOR were detected by western blot, and cell metabolic was analyzed by seahorse.Results: Large numbers of CD68+ macrophages gathered in close liver issue from the lesion in AE patients. PSCs preferentially differentiated into M2 macrophages and the expressions of HK1, PFKL, PKM2, PI3K, pAKT, and mTOR increased with the extension of co-culture time.Conclusions: Echinococcus multilocularis protoscoleces enhance glycolysis to promote M2 macrophages through PI3K/Akt/mTOR signaling pathway.