mmu-miR-374b-5p modulated inflammatory factors via downregulation of C/EBP β/NF-κB signaling in Kupffer cells during Echinococcus multilocularis infection

文献类型： 外文期刊

第一作者： Pu, Guiting

作者： Pu, Guiting;Li, Yanping;Liu, Tingli;Li, Hong;Wang, Liqun;Chen, Guoliang;Cao, Shanling;Yin, Hong;Amuda, Tharheer Oluwashola;Guo, Xiaola;Luo, Xuenong;Yin, Hong;Luo, Xuenong

作者机构：

关键词： Echinococcus multilocularis; miR-374b-5p; Inflammatory factors; C/EBP beta; NF-kappa B

期刊名称：PARASITES & VECTORS （ 影响因子：3.2； 五年影响因子：3.6 ）

ISSN： 1756-3305

年卷期： 2024 年 17 卷 1 期

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收录情况： SCI

摘要： Background Alveolar echinococcosis (AE) is an important infectious disease caused by the metacestode larvae of Echinococcus multilocularis, seriously threatening global public health security. Kupffer cells (KCs) play important roles in liver inflammatory response. However, their role in hepatic alveolar echinococcosis has not yet been fully elucidated. Methods In this study, qRT-PCR was used to detect the expression level of miR-374b-5p in KCs. The target gene of miR-374b-5p was identified through luciferase reporter assays and loss of function and gains. Critical genes involved in NF kappa B signaling pathway were analyzed by qRT-PCR and western blot. Results This study reported that miR-374b-5p was significantly upregulated in KCs during E. multilocularis infection and further showed that miR-374b-5p was able to bind to the 3'-UTR of the C/EBP beta gene and suppressed its expression. The expression levels of NF-kappa Bp65, p-NF-kappa Bp65 and pro-inflammatory factors including iNOS, TNF alpha and IL6 were attenuated after overexpression of miR-374b-5p while enhanced after suppression of miR-374b-5p. However, the Arg1 expression level was promoted after overexpression of miR-374b-5p while suppressed after downregulation of miR-374b-5p. Additionally, increased protein levels of NF-kappa Bp65 and p-NF-kappa Bp65 were found in the C/EBP beta-overexpressed KCs. Conclusions These results demonstrated that miR-374b-5p probably regulated the expression of inflammatory factors via C/EBP beta/NF-kappa B signaling. This finding is helpful to explore the mechanism of inflammation regulation during E. multilocularis infection.

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