自噬
PI3K/AKT/mTOR通路
无乳链球菌
细胞内
蛋白激酶B
细胞生物学
微生物学
程序性细胞死亡
生物
化学
信号转导
细胞凋亡
链球菌
生物化学
细菌
遗传学
作者
Mengzhu Qi,Hao Geng,Na Geng,Yukun Cui,Changxi Qi,Guodong Cheng,Kaimin Song,Liping Hu,Yongxia Liu,Jianzhu Liu,Bo Han
出处
期刊:Journal of Dairy Research
[Cambridge University Press]
日期:2022-04-07
卷期号:89 (2): 178-184
被引量:7
标识
DOI:10.1017/s0022029922000243
摘要
Abstract Streptococcus agalactiae ( S. agalactiae ) infection is a significant cause of mastitis, resulting in loss of cellular homeostasis and tissue damage. Autophagy plays an essential function in cell survival, defense, and the preservation of cellular homeostasis, and is often part of the response to pathogenic challenge. However, the effect of autophagy induced by S. agalactiae in bovine mammary epithelial cells (bMECs) is mainly unknown. So in this study, an intracellular S. agalactiae infection model was established. Through evaluating the autophagy-related indicators, we observed that after S. agalactiae infection, a significant quantity of LC3-I was converted to LC3-II, p62 was degraded, and levels of Beclin1 and Bcl2 increased significantly in bMECs, indicating that S. agalactiae induced autophagy. The increase in levels of LAMP2 and LysoTracker Deep Red fluorescent spots indicated that lysosomes had participated in the degradation of autophagic contents. After autophagy was activated by rapamycin (Rapa), the amount of p-Akt and p-mTOR decreased significantly, whilst the amount of intracellular S. agalactiae increased significantly. Whereas the autophagy was inhibited by 3-methyladenine (3MA), the number of intracellular pathogens decreased. In conclusion, the results demonstrated that S. agalactiae could induce autophagy through PI3K/Akt/mTOR pathway and utilize autophagy to survive in bMECs.
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