Suppr超能文献

产气荚膜梭菌β2 毒素刺激 IPEC-J2 细胞中 JAK/STAT 通路的分子特征和功能。

Molecular characterization and function of JAK/STAT pathway in IPEC-J2 cells during Clostridium perfringens beta2 toxin stimulation.

机构信息

College of Animal Science and Technology, Gansu Agricultural University, Lanzhou, 730070, China.

Farmer Education and Training Work Station of Gansu province, Lanzhou, 730070, China.

出版信息

Vet Res Commun. 2023 Sep;47(3):1177-1184. doi: 10.1007/s11259-023-10118-w. Epub 2023 Jul 12.

Abstract

Intestinal infection with C. perfringens is responsible for outbreaks of diarrhea in piglets. Janus kinase / signal transducer and activator of transcription (JAK/STAT) is a vital signaling pathway that regulates cellular activity and inflammatory response, closely correlated with multiple diseases development and advances. Currently, the potential effect of JAK/STAT on C. perfringens beta2 (CPB2) treatment on porcine intestinal epithelial (IPEC-J2) cells has not been explored. The expression of JAK/STAT genes or proteins in IPEC-J2 cells induced by CPB2 were observed by qRT-PCR and Western blot, and further used WP1066 to explore the effect of JAK2/STAT3 on mechanism employed by CPB2 on apoptosis, cytotoxicity, oxidative stress and inflammatory cytokines of IPEC-J2 cells. JAK2, JAK3, STAT1, STAT3, STAT5A and STAT6 were highly expressed in CPB2-induced IPEC-J2 cells, among which STAT3 had the highest expression. Moreover, apoptosis, cytotoxicity and oxidative stress were attenuated via blocking the activation of JAK2/STAT3 by using WP1066 in CPB2-treated IPEC-J2 cells. Furthermore, WP1066 significantly suppressed the secretion of interleukin (IL)-6, IL-1β and TNF-α induced by CPB2 in IPEC-J2 cells.Our findings provide some insights into the functional roles of JAK2/STAT3 in piglets against to C. perfringens infection.

摘要

产气荚膜梭菌引起的肠道感染可导致仔猪腹泻暴发。Janus 激酶/信号转导子和转录激活子(JAK/STAT)是一种重要的信号通路,调节细胞活性和炎症反应,与多种疾病的发生和进展密切相关。目前,尚未探讨 JAK/STAT 对产气荚膜梭菌β2(CPB2)治疗猪肠上皮(IPEC-J2)细胞的潜在影响。通过 qRT-PCR 和 Western blot 观察 CPB2 诱导的 IPEC-J2 细胞中 JAK/STAT 基因或蛋白的表达,并进一步使用 WP1066 探讨 JAK2/STAT3 对 CPB2 诱导的 IPEC-J2 细胞凋亡、细胞毒性、氧化应激和炎症细胞因子的作用机制。CPB2 诱导的 IPEC-J2 细胞中 JAK2、JAK3、STAT1、STAT3、STAT5A 和 STAT6 表达较高,其中 STAT3 表达最高。此外,通过 WP1066 阻断 JAK2/STAT3 的激活,可减轻 CPB2 处理的 IPEC-J2 细胞中的凋亡、细胞毒性和氧化应激。此外,WP1066 显著抑制 CPB2 诱导的 IPEC-J2 细胞中白细胞介素(IL)-6、IL-1β 和 TNF-α 的分泌。我们的研究结果为 JAK2/STAT3 在仔猪抵抗产气荚膜梭菌感染中的功能作用提供了一些见解。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验