PI3K/AKT/mTOR通路
多房棘球绦虫
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
川地68
信号转导
包虫病
巨噬细胞
免疫学
医学
病理
新陈代谢
内分泌学
生物化学
免疫组织化学
体外
作者
Tao Zhang,Yuegang Zhang,Zihan Yang,Yuan Jiang,Li Sun,Dengliang Huang,Meiyuan Tian,Yinhong Shen,Jun Deng,Jing Hou,Yanyan Ma
标识
DOI:10.1080/20477724.2022.2104055
摘要
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. We found that 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, Akt, p-Akt, mTOR and p-mTOR increased. The above results show that Echinococcus multilocularis protoscoleces enhance glycolysis to promote M2 macrophages through PI3K/Akt/mTOR signaling pathway.
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