Exosomal tpi-miR-10a-5p from T. pisiformis cysticerci regulates the expression of inflammatory factors in rabbits by targeting MAP3K7

文献类型： 外文期刊

第一作者： Pu, Guiting

作者： Pu, Guiting;Wang, Liqun;Liu, Tingli;Wang, Dexian;Li, Hong;Amuda, Tharheer Oluwashola;Yin, Hong;Yan, Hongbin;Luo, Xuenong;Zhang, Xueyong;Yin, Hong;Luo, Xuenong;Pu, Guiting

作者机构：

关键词： T. pisiformis cysticerci; Exosome; Tpi-miR-10a-5p; Rabbits

期刊名称：VETERINARY PARASITOLOGY （ 影响因子：2.2； 五年影响因子：2.4 ）

ISSN： 0304-4017

年卷期： 2025 年 338 卷

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收录情况： SCI

摘要： Taenia pisiformis (T. pisiformis) cysticerci, belonging to Taeniidae, attaches to the wall of the mesentery and omentum of rabbits, causing cysticercosis pisiformis that can seriously affect the healthy development of the rabbit breeding industry. Helminths can produce exosomes containing proteins and RNAs. In our previous study, tpi-miR-10a-5p was found to be highly enriched in the exosomes from T. pisiformis cysticerci. In this study, we report that tpi-miR-10a-5p is significantly up-regulated in the blood and peripheral blood lymphocytes (PBLCs) of T. pisiformis-infected rabbits. Furthermore, tpi-miR-10a-5p targets mitogen-activated protein kinase kinase kinase 7 (MAP3K7), the key gene involved in the c-Jun N-terminal kinase (JNK) signaling pathway. Knockdown of MAP3K7 inhibited the JNK signaling pathway, suppressing the production of inflammatory cytokines such as IFN-gamma and TNF alpha, whereas overexpression of MAP3K7 activated the JNK signaling pathway in PBLCs. The same trend was observed with knockdown of MAP3K7 when PBLCs were treated with exosomes from T. pisiformis cysticerci. In vivo experiment further demonstrated that the expression of MAP3K7, JNK, p-JNK, IFN-gamma, and TNF alpha was significantly decreased in PBLCs during T. pisiformis infection. Therefore, tpi-miR-10a-5p can suppress the JNK signaling pathway and inflammatory response by targeting MAP3K7 in host PBLCs. These findings may imply a mechanism used by the parasites releasing exosomes to sense and adapt to the host environment by regulating the immune reaction.

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