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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.

DOI:10.1007/s11259-023-10118-w
PMID:37436554
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。

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本文引用的文献

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Comparative Transcriptome Profiling of Human and Pig Intestinal Epithelial Cells after Porcine Deltacoronavirus Infection.猪德尔塔冠状病毒感染后人肠上皮细胞和猪肠上皮细胞的比较转录组学分析。
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Human gene expression profiling identifies key therapeutic targets in tuberculosis infection: A systematic network meta-analysis.人类基因表达谱分析确定结核感染的关键治疗靶点:系统网络荟萃分析。
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Clostridium perfringens beta2 toxin induced in vitro oxidative damage and its toxic assessment in porcine small intestinal epithelial cell lines.
产气荚膜梭菌β2 毒素诱导的体外氧化损伤及其对猪小肠上皮细胞系的毒性评估。
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Interference with miR-210 Alleviated Renal Injury in Septic Rats by Inhibiting JAK-STAT Pathway.miR-210 干扰通过抑制 JAK-STAT 通路减轻脓毒症大鼠的肾损伤。
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Incidence of Clostridium perfringens and its toxin genes in the gut of children with autism spectrum disorder.自闭症谱系障碍儿童肠道中产气荚膜梭菌及其毒素基因的发生率。
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and protective effect of arginine against intestinal inflammatory response induced by in broiler chickens.以及精氨酸对肉鸡肠道炎症反应的保护作用。 你提供的原文似乎不完整,“induced by”后面缺少具体内容。
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