自噬
粪肠球菌
脂磷壁酸
PI3K/AKT/mTOR通路
蛋白激酶B
微生物学
化学
细胞生物学
生物
细菌
信号转导
金黄色葡萄球菌
生物化学
细胞凋亡
基因
大肠杆菌
遗传学
作者
Dagui Lin,Gao Yan,Li Zhao,Yanhuo Chen,Shengli An,Zhixiang Peng
标识
DOI:10.1016/j.bbrc.2018.03.109
摘要
Enterococcus faecalis (E. faecalis) infection is considered an important etiological factor for the development of persistent apical periodontitis (PAP), but the exact mechanisms of autophagy between E. faecalis and immune cells remain unknown. In this study, we elucidated how E. faecalis lipoteichoic acid (LTA) is associated with macrophages autophagy. We found that E. faecalis LTA apparently activated macrophage autophagy with significant increase of autophagosomes and autophagy relative protein. Meanwhile, we noticed significantly decreasing expression of p-Akt and p-mTOR. However, these effect were absent in macrophages knockdown of Beclin1. In summary, these findings suggested E. faecalis LTA may increased macrophages autophagy via inhibiting PI3K/Akt/mTOR pathway and this process was Beclin1 dependent.
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