[目的]探究小反刍兽疫病毒(Peste des petits ruminants virus，PPRV)感染引起的炎症反应并解析其致病机制。[方法]分离山羊肺泡巨噬细胞(PAM)，利用qRT-PCR、ELISA及组织病理切片HE染色等方法分别检测PPRV感染后引起的炎性细胞因子表达、一氧化氮(NO)含量和炎性细胞侵润等现象。进一步利用转录组学测序分析PPRV感染PAM引起的差异基因、信号通路以及差异基因的表达情况。[结果]与正常山羊相比，感染PPRV的山羊其肝脏、肾脏及肺脏的部分细胞坏死并且呈现炎性细胞侵润的现象;与对照组相比，感染后的PAM细胞显著增加了 NO含量(P＜0。001);与未感染组相比，PPRV感染的PAM其炎性细胞因子IL-1β、TNF-α、IL-10等mRNA表达水平显著升高(P＜0。05);此外，PPRV感染诱导的差异基因主要集中在炎症通路及NF-κB信号通路等。[结论]PPRV通过诱导大量炎性细胞侵润、增加炎性细胞因子表达，激活炎症信号通路从而产生炎症反应。
PPRV induces an inflammatory response in macrophages
[Objective]To explore the inflammatory response caused by peste des petits ruminants virus(PPRV)infection and its pathogenic mechanism.[Method]Goat alveolar macrophages(PAM)were isolated.The expression of inflammatory cyto-kines,the content of nitric oxide(NO),and the infiltration of inflammatory cells were detected by qRT-PCR,ELISA,and he-matoxylin-and-eosin(H&E)staining.Furthermore,transcriptome sequencing was used to analyze the differentially ex-pressed genes,signal pathways,and the expression of differentially expressed genes in PPRV-infected PAM cells.[Result]Compared to normal goats,there were some cells in the liver,kidney,and lung of PPRV infected goats which presented with the necrotic inflammty cell.Compared with the control group,the expression of NO in PPRV-infected PAM increased significantly(P＜0.001),and the expression of IL-1β,TNF-α,and IL-10 also increased after PPRV infection(P＜0.05).Besides,the differentially expressed genes were mainly enriched in the inflammation pathway and NF-κB signaling pathway.[Conclusion]PPRV causes inflammatory response by inducing some scattered inflammatory cells,increasing the expression of inflammatory cytokines,and activating inflammatory signaling pathways.
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