Institute of Immunology and Molecular Medicine, Jining Medical University, Jining, China.
Jining Key Laboratory of Immunology, Jining Medical University, Jining, China.
mBio. 2023 Dec 19;14(6):e0209423. doi: 10.1128/mbio.02094-23. Epub 2023 Nov 1.
Kidney injury during acute urinary tract infections (UTIs) caused by uropathogenic (UPEC) is an important public health problem. However, how kidney injury develops during UPEC infection is still unclear. Although antibiotic therapy is currently an effective treatment for UTI, it cannot avoid kidney injury. MicroRNAs have gained extensive attention as essential molecules capable of regulating the autoimmune response. Among these, microRNA-146b (miR-146b) is involved in regulating inflammatory responses. In the present study, we demonstrated that miR-146b played an essential role in the development of kidney injury during UTIs caused by UPEC. The results showed that miR-146b may suppress M1 macrophage polarization and alleviate acute kidney injury. Furthermore, the miR-146b activator, agomir, in order to upregulate miR-146b, was effective in treating kidney damage by inhibiting the activation of M1 macrophages. In conclusion, our findings elucidated the mechanisms by which miR-146b alleviated kidney injury induced by UTIs, shed new light on the relationship between microRNA and bacterial infection, and provided a novel therapeutic target for treating this common bacterial infection.
在由尿路致病性大肠杆菌(UPEC)引起的急性尿路感染(UTI)期间发生的肾脏损伤是一个重要的公共卫生问题。然而,在 UPEC 感染期间肾脏损伤如何发展仍不清楚。尽管抗生素治疗目前是治疗 UTI 的有效方法,但它不能避免肾脏损伤。microRNAs 作为能够调节自身免疫反应的重要分子引起了广泛关注。其中,microRNA-146b(miR-146b)参与调节炎症反应。在本研究中,我们证明 miR-146b 在 UPEC 引起的 UTI 期间肾脏损伤的发展中起着重要作用。结果表明,miR-146b 可能抑制 M1 巨噬细胞极化并减轻急性肾损伤。此外,miR-146b 激活剂 agomir 上调 miR-146b 可通过抑制 M1 巨噬细胞的激活来有效治疗肾脏损伤。总之,我们的研究结果阐明了 miR-146b 缓解 UTI 引起的肾脏损伤的机制,为 microRNA 与细菌感染之间的关系提供了新的认识,并为治疗这种常见的细菌感染提供了新的治疗靶点。