文献类型： 外文期刊

作者： Deng, Ziteng ¹ ; Sun, Qian ¹ ; Li, Shun ¹ ; Wang, Yibo ¹ ; Che, Yuxin ¹ ; Huang, Yunfei ¹ ; Liao, Jiedan ¹ ; Xie, Honglin ¹ ; Zhan, Xiaoshu ¹ ; Sun, Qinqin ¹ ; Fu, Qiang ¹ ;

作者机构： 1.Foshan Univ, Sch Anim Sci & Technol, 33 Guangyun Rd, Foshan 528225, Peoples R China

2.Foshan Univ, Vet Teaching Hosp, Foshan 528225, Peoples R China

3.Xinjiang Acad Agr & Reclamat Sci, Kunyu Integrated Agr Res Inst, Shihezi 848116, Peoples R China

关键词： Streptococcus suis type 2; macrophage; NLRP3; miR-7a-5p; inflammation

期刊名称：MICROORGANISMS （ 影响因子：4.2； 五年影响因子：4.6 ）

ISSN：

年卷期： 2025 年 13 卷 8 期

页码：

收录情况： SCI

摘要： Streptococcus suis type 2 (SS2) is a pathogen causing diseases like meningitis and septicaemia worldwide. While microRNAs (miRNAs) are acknowledged for their role in post-transcriptional regulation of gene expression and influence on immune responses, their exact functions in hosts during SS2 infection remain elusive. This study aims to explore the role of miR-7a-5p in macrophages during SS2 infection. Our findings reveal that SS2 infection in J774A.1 cells triggers upregulation of the NLRP3 inflammasome signaling pathways, evidenced by enhanced mRNA expression of pro-inflammatory cytokines (IL-6, IL-18, IL-23, TNF-alpha) and elevated protein levels of NLRP3, caspase-1, and IL-1 beta. Concurrently, SS2 infection reduces miR-7a-5p expression. Dual-luciferase reporter assays confirm that miR-7a-5p directly targets the 3 ' UTR of NLRP3 mRNA. Notably, miR-7a-5p overexpression in SS2-infected J774A.1 cells suppresses NLRP3 inflammasome activation and downstream signaling, as demonstrated by reduced mRNA levels of inflammatory mediators and decreased protein levels of NLRP3, caspase-1, IL-1 beta, and IL-18. Conversely, miR-7a-5p inhibition produces effects opposite to those of overexpression. In mice, administration of miR-7a-5p mimics mitigates SS2-induced lung, liver, and spleen damage, reducing histological scores in these organs. Collectively, these results show that miR-7a-5p alleviates SS2-induced inflammation by inhibiting the NLRP3 inflammasome, underscoring its potential as a therapeutic target for SS2-associated diseases.