Domain fusion TLR2-4 enhances the autophagy-dependent clearance of Staphylococcus aureus in the genetic engineering goat
文献类型： 外文期刊
作者： Wang, Mengyao 1 ; Qi, Yu 1 ; Cao, Yutao 1 ; Zhang, Xiaosheng 4 ; Wang, Yongsheng 5 ; Liu, Qingyou 6 ; Zhang, Jinlong 4 ; Zhou, Guangbin 7 ; Ai, Yue 1 ; Wei, Shao 1 ; Wang, Linli 1 ; Liu, Guoshi 1 ; Lian, Zhengxing 1 ; Han, Hongbing 1 ;
作者机构： 1.China Agr Univ, Coll Anim Sci & Technol, Beijing Key Lab Anim Genet Improvement, Beijing, Peoples R China
2.China Agr Univ, Coll Anim Sci & Technol, Natl Engn Lab Anim Breeding, Beijing, Peoples R China
3.China Agr Univ, Coll Anim Sci & Technol, Key Lab Anim Genet Breeding & Reprod, Minist Agr & Rural Affairs, Beijing, Peoples R China
4.Tianjin Acad Agr Sci, Tianjin, Peoples R China
5.Northwest Agr & Forest Univ, Key Lab Anim Biotechnol, Minist Agr, Xianyang, Shaanxi, Peoples R China
6.Guangxi Univ, State Key Lab Conservat & Utilizat Subtrop Agrobio, Nanning, Peoples R China
7.Sichuan Agr Univ, Coll Anim Sci & Technol, Farm Anim Genet Resources Explorat & Innovat Key L, Chengdu, Peoples R China
关键词： Toll-like receptor 2-4; Staphylococcus aureus; autophagy; macrophages; goat; Other
期刊名称：ELIFE （ 影响因子：8.713； 五年影响因子：9.393 ）
ISSN： 2050-084X
年卷期： 2022 年 11 卷
页码：
收录情况： SCI
摘要： Staphylococcus aureus infections pose a potential threat to livestock production and public health. A novel strategy is needed to control S. aureus infections due to its adaptive evolution to antibiotics. Autophagy plays a key role in degrading bacteria for innate immune cells. In order to promote S. aureus clearance via Toll-like receptor (TLR)-induced autophagy pathway, the domain fusion TLR2-4 with the extracellular domain of TLR2, specific recognizing S. aureus, and transmembrane and intracellular domains of TLR4 is assembled, then the goat expressing TLR2-4 is generated. TLR2-4 substantially augments the removal of S. aureus within macrophages by elevating autophagy level. Phosphorylated JNK and ERK1/2 promote LC3-puncta in TLR2-4 macrophages during S. aureus-induced autophagy via MyD88 mediated the TAK1 signaling cascade. Meantime, the TRIF-dependent TBK1-TFEB-OPTN signaling is involved in TLR2-4-triggered autophagy after S. aureus challenge. Moreover, the transcript of ATG5 and ATG12 is significantly increased via cAMP-PKA-NF-kappa B signaling, which facilitates S. aureus-induced autophagy in TLR2-4 macrophages. Overall, the novel receptor TLR2-4 enhances the autophagy-dependent clearance of S. aureus in macrophages via TAK1/TBK1-JNK/ERK, TBK1-TFEB-OPTN, and cAMP-PKA-NF-kappa B-ATGs signaling pathways, which provide an alternative approach for resistant against S. aureus infection.
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