Porcine Epidemic Diarrhea Virus Infection of Porcine Intestinal Epithelial Cells Causes Mitochondrial DNA Release and the Activation of the NLRP3 Inflammasome to Mediate Interleukin-1β Secretion

文献类型： 外文期刊

第一作者： Bao, Di

作者： Bao, Di;Zhao, Han;Liu, Jiuyuan;Wei, Yiming;Hu, Guixue;Yi, Shushuai;Zhao, Luobing;Liu, Xinxin

作者机构：

关键词： PEDV; mtDNA; NLRP3; IPEC-J2; IL-1 beta; inflammation

期刊名称：VETERINARY SCIENCES （ 影响因子：2.3； 五年影响因子：2.4 ）

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年卷期： 2024 年 11 卷 12 期

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收录情况： SCI

摘要： Porcine epidemic diarrhea virus (PEDV) induces enteritis and diarrhea in piglets. Mitochondrial DNA (mtDNA) contributes to virus-induced inflammatory responses; however, the involvement of inflammasomes in PEDV infection responses remains unclear. We investigated the mechanism underlying inflammasome-mediated interleukin (IL)-1 beta secretion during the PEDV infection of porcine intestinal epithelial (IPEC-J2) cells. IL-1 beta production and caspase-1 activity were assessed by quantitative PCR and enzyme-linked immunosorbent assay. NLRP3 inflammasome activation was assessed using immunoprecipitation experiments. Mitochondrial damage was evaluated by analyzing the mitochondrial membrane potential and ATP levels and by the flow cytometry examination of mitochondrial reactive oxygen species (mtROS). Mitochondria and mtDNA localization were observed using immunofluorescence. The inhibition of mtROS and mtDNA production allowed NLRP3 inflammasome and IL-1 beta expression detection and the evaluation of the pathway underlying NLRP3 inflammasome activation in PEDV-infected IPEC-J2 cells. IPEC-J2 cells upregulated IL-1 beta upon PEDV infection, where mature IL-1 beta secretion depended on caspase-1 activity, triggered NLRP3 inflammasome expression and assembly, and caused mitochondrial dysfunction, leading to mtDNA release and NLRP3 inflammasome activation, while mtROS contributed to NF-kappa B pathway activation, enhancing IL-1 beta secretion. This is the first demonstration of the mechanism underlying mtDNA release and NLRP3 inflammasome activation facilitating IL-1 beta secretion from PEDV-infected IPEC-J2 cells. These data enhance our understanding of the inflammatory mechanisms triggered by PEDV.

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