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

第一作者： Wang, Mengyao

作者： Wang, Mengyao;Qi, Yu;Cao, Yutao;Ai, Yue;Wei, Shao;Wang, Linli;Liu, Guoshi;Lian, Zhengxing;Han, Hongbing;Wang, Mengyao;Qi, Yu;Cao, Yutao;Ai, Yue;Wei, Shao;Wang, Linli;Liu, Guoshi;Lian, Zhengxing;Han, Hongbing;Wang, Mengyao;Qi, Yu;Cao, Yutao;Ai, Yue;Wei, Shao;Wang, Linli;Liu, Guoshi;Lian, Zhengxing;Han, Hongbing;Zhang, Xiaosheng;Zhang, Jinlong;Wang, Yongsheng;Liu, Qingyou;Zhou, Guangbin

作者机构：

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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