循环氧化酶-2/前列腺素E2通路调节鸟类巨细胞中传染性支气管炎病毒的复制
Motamed Elsayed Mahmoud1,2, Muhammad Farooq1, Ishara M Isham1
1Faculty of Veterinary Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada.
The Journal of general virology
|January 8, 2024
概括
传染性支气管炎病毒 (IBV) 在巨中增强循环氧化酶-2 (COX-2) 和前列腺素E2 (PGE2),帮助病毒复制. 抑制这种途径可以增强巨细胞对IBV的防御能力,降低病毒载量.
科学领域:
- 鸟类免疫学 鸟类免疫学
- 病毒学 病毒学
- 分子生物学分子生物学
背景情况:
- 传染性支气管炎病毒 (IBV) 是一个重要的鸟类呼吸道病原体.
- 的巨细胞是IBV的先天免疫反应中的关键细胞.
- IBV对巨细胞中循环氧化酶-2 (COX-2) 和前列腺素E2 (PGE2) 的影响尚不清楚.
研究的目的:
- 调查IBV感染在巨中COX-2和PGE2产生中的作用.
- 为了确定抑制COX-2/PGE2通路对IBV复制的作用.
- 探索COX-2/PGE2对其他免疫媒介,如iNOS和IL-6的影响.
主要方法:
- 巨细胞培养物感染了两个IBV菌株.
- 细胞内和细胞外IBV,COX-2和PGE2.2的量化.
- 选择性COX-2抗剂和PGE2受体 (EP2,EP4) 抑制剂的使用.
- 诱导性氧化合成酶 (iNOS),氧化 (NO) 和中白素-6 (IL-6) 表达的评估.
主要成果:
- IBV感染在mRNA和蛋白质水平上显著增加了COX-2和PGE2的产生.
- 抑制COX-2或PGE2受体可以减少IBV复制.
- 外源性PGE2增强了病毒复制,而其抑制则减少了病毒复制.
- IBV感染上调了iNOS,NO和IL-6;COX-2/PGE2通路的抑制降低了这些媒介.
结论:
- IBV感染操纵巨中的COX-2/PGE2通路,以促进病毒复制.
- 抑制COX-2/PGE2通路可以增强巨细胞对IBV的抗病毒防御能力.
- 准COX-2/PGE2通路是控制IBV感染的潜在策略.
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