多房棘球绦虫
PI3K/AKT/mTOR通路
蛋白激酶B
糖酵解
生物
巨噬细胞极化
癌症研究
细胞生物学
免疫印迹
川地68
信号转导
巨噬细胞
包虫病
免疫学
新陈代谢
生物化学
免疫组织化学
基因
体外
动物
作者
Tao Zhang,Yuegang Zhang,Zihan Yang,Yuan Jiang,Li Sun,Dengliang Huang,Meiyuan Tian,Yinhong Shen,Jun Deng,Jin Hou,Yanyan Ma
出处
期刊:Research Square - Research Square
日期:2022-05-20
被引量:1
标识
DOI:10.21203/rs.3.rs-1665573/v1
摘要
Abstract 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.
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