APEC infection affects cytokine-cytokine receptor interaction and cell cycle pathways in chicken trachea

APEC infection affects cytokine-cytokine receptor interaction and cell cycle pathways in chicken trachea
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APEC 感染影响鸡气管中细胞因子-细胞因子受体相互作用和细胞周期途径。

DOI:
10.1016/j.rvsc.2020.03.016
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发表时间:
2020-06-01
影响因子:
2.4
通讯作者:
Qi, Kezong
Qi, Kezong
中科院分区:
农林科学3区
文献类型:
--
作者:
Song, Xiangjun;Jiang, Huyan;Qi, Kezong

文献摘要

被引文献

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禽病原性大肠杆菌(APEC)可通过呼吸道感染导致鸟类肠道外疾病。然而,APEC对鸡气管上皮细胞致病性的调控机制尚不清楚。本实验研究了不同感染时间(4、8、12和24 h)鸡气管的病理变化。对APEC感染组和PBS组(阴性对照)鸡气管上皮细胞进行RNA测序分析。结果表明,感染后8和12 h,肺组织出现水肿、嗜异细胞浸润和充血。感染后24 h,充血现象和嗜异性粒细胞浸润消失。RNA测序结果显示,APEC感染组中有多个基因动态表达。感染后4、8和12 h,差异表达基因的mRNA通过嘌呤-细胞因子受体相互作用和toll样受体信号通路富集。细胞周期途径在感染后24 h富集。总之,这些研究结果表明,APEC感染诱导鸡气管,参与炎症和增生信号通路的差异表达基因的mRNA的病理变化。这不仅为APEC对鸡气管上皮细胞致病性的调控机制提供了更多的证据,也为有效控制禽经气管感染APEC提供了理论依据。
Avian pathogenic Escherichia coil (APEC) can lead to extraintestinal disease in avian species via respiratory tract infection. However, the regulatory mechanism of APEC on the pathogenicity of chicken trachea epithelium remains unknown. In this study, we examined pathological changes in chicken trachea at different infection times (4, 8, 12 and 24 h). The RNA sequencing of APEC infection group and the PBS group (negative control) of chicken trachea epithelium were analysed. Our studies revealed that the oedema, heterophil infiltration and hyperaemia appeared at 8 and 12 h post APEC infection. And the hyperaemia phenomenon and heterophilic granulocyte infiltration disappeared at 24 h post infection. Then RNA sequencing showed many genes were dynamically expressed in the APEC infection group. M 4, 8 and 12 h post infection, the mRNA of differentially expressed genes were enriched by cytokine-cytokine receptor interaction and the toll-like receptor signalling pathway. The cell cycle pathway was enriched at 24 h post infection. Altogether, these findings suggest that APEC infection induces pathological change in the chicken trachea, the mRNA of differentially expressed genes participating in inflammation and hyperplasia signalling pathways. Which not only provide more evidence for regulatory mechanism of APEC on the pathogenicity of chicken trachea epithelium, but also facilitate the effective management of APEC infections in poultry through trachea.