文献类型： 外文期刊
作者： Jiang, Changsheng 1 ; Zhou, Pei 1 ; Zhang, Xiaoqian 2 ; Ma, Ningning 1 ; Hu, Yaofang 1 ; Zhang, Mengjia 1 ; Ghonaim, Ahmed H. 1 ; Li, Huimin 1 ; Dong, Ling 1 ; Zeng, Wei 4 ; Li, Chang 5 ; Lang, Yifei 6 ; Sun, Yumei 1 ; He, Qigai 1 ; Li, Wentao 1 ;
作者机构： 1.Huazhong Agr Univ, Coll Anim Sci & Vet Med, Cooperat Innovat Ctr Sustainable Pig Prod, Natl Key Lab Agr Microbiol, Wuhan 430070, Peoples R China
2.China Inst Vet Drug Control, Beijing 102629, Peoples R China
3.Desert Res Ctr, Cairo 11435, Egypt
4.Hubei Acad Agr Sci, Hubei Key Lab Anim Embryo Engn & Mol Breeding, Wuhan 430064, Peoples R China
5.Hubei Acad Agr Sci, Inst Anim Husb & Vet, Key Lab Prevent & Control Agents Anim Bacteriosis, Minist Agr & Rural Affairs, Wuhan 430064, Peoples R China
6.Sichuan Agr Univ, Coll Vet Med, Chengdu 611130, Peoples R China
7.Hubei Hongshan Lab, Wuhan 430070, Peoples R China
关键词： Apoptosis; ARF6; p38 MAPK signaling pathway; Streptococcus suis; Suilysin; TurboID-mediated proximity labeling
期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：7.7； 五年影响因子：7.7 ）
ISSN： 0141-8130
年卷期： 2024 年 268 卷
页码：
收录情况： SCI
摘要： Streptococcus suis (S. suis) is a significant zoonotic microorganism that causes a severe illness in both pigs and humans and is characterized by severe meningitis and septicemia. Suilysin (SLY), which is secreted by S. suis, plays a crucial role as a virulence factor in the disease. To date, the interaction between SLY and host cells is not fully understood. In this study, we identified the interacting proteins between SLY and human brain microvascular endothelial cells (HBMECs) using the TurboID-mediated proximity labeling method. 251 unique proteins were identified in TurboID-SLY treated group, of which six plasma membrane proteins including ARF6, GRK6, EPB41L5, DSC1, TJP2, and PNN were identified. We found that the proteins capable of interacting with SLY are ARF6 and PNN. Subsequent investigations revealed that ARF6 substantially increased the invasive ability of S. suis in HBMECs. Furthermore, ARF6 promoted SLY-induced the activation of p38 MAPK signaling pathway in HBMECs. Moreover, ARF6 promoted the apoptosis in HBMECs through the activation of p38 MAPK signaling pathway induced by SLY. Finally, we confirmed that ARF6 could increase the virulence of SLY in C57BL/6 mice. These findings offer valuable insights that contribute to a deeper understanding of the pathogenic mechanism of SLY.
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