H9N2甲型流感病毒感染后，铜绿假单胞菌脂多糖的刺激会加剧肺泡巨噬细胞的炎症反应并减少病毒复制。
Stimulation of lipopolysaccharide from Pseudomonas aeruginosa following H9N2 IAV infection exacerbates inflammatory responses of alveolar macrophages and decreases virus replication.
作者信息
Shun Kang, Ying-Li Sun, Zhi-Juan Li, Jian-Liang Li, Feng Xiao, Lu-Jiao Dong, Peng Yuan, Jiang Shijin, Zhi-Jing Xie
机构信息
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, Taian, Shandong Province, 271018, China; College of Veterinary Medicine, Shandong Agricultural University, Taian, Shandong Province, 271018, China.
Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, Taian, Shandong Province, 271018, China; College of Veterinary Medicine, Shandong Agricultural University, Taian, Shandong Province, 271018, China; Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, Taian, Shandong Province, 271018, China.
出版信息
Microb Pathog. 2023 Sep;182:106254. doi: 10.1016/j.micpath.2023.106254. Epub 2023 Jul 21.
H9N2 IAV infection contributed to P. aeruginosa coinfection, causing severe hemorrhagic pneumonia in mink. In this study, the in vitro alveolar macrophage models were developed to investigate the innate immune responses to P. aeruginosa LPS stimulation following H9N2 IAV infection, using MH-S cells. The cytokine levels, apoptosis levels and the viral nucleic acid levels were detected and analyzed. As a result, the levels of IFN-α, IL-1β, TNF-α, and IL-10 in MH-S cells with P. aeruginosa LPS stimulation following H9N2 IAV infection were significantly higher than those in MH-S cells with single H9N2 IAV infection and single LPS stimulation (P < 0.05), exacerbating inflammatory responses. LPS stimulation aggravated the apoptosis of MH-S cells with H9N2 IAV infection. Interestingly, LPS stimulation influences H9N2 IAV replication and indirectly reduced H9N2 IAV replications in in vitro AMs. It implied that LPS should play an important role in the pathogenesis of H9N2 IAV and P. aeruginosa coinfection.
H9N2 甲型流感病毒感染导致铜绿假单胞菌合并感染，引发水貂严重出血性肺炎。在本研究中，利用 MH-S 细胞建立体外肺泡巨噬细胞模型，以研究 H9N2 甲型流感病毒感染后对铜绿假单胞菌脂多糖刺激的天然免疫反应。检测并分析了细胞因子水平、凋亡水平和病毒核酸水平。结果显示，H9N2 甲型流感病毒感染后经铜绿假单胞菌脂多糖刺激的 MH-S 细胞中，IFN-α、IL-1β、TNF-α 和 IL-10 的水平显著高于单纯 H9N2 甲型流感病毒感染和单纯脂多糖刺激的 MH-S 细胞（P < 0.05），加剧了炎症反应。脂多糖刺激加重了 H9N2 甲型流感病毒感染的 MH-S 细胞的凋亡。有趣的是，脂多糖刺激影响 H9N2 甲型流感病毒复制，并间接降低了体外肺泡巨噬细胞中 H9N2 甲型流感病毒的复制。这表明脂多糖在 H9N2 甲型流感病毒和铜绿假单胞菌合并感染的发病机制中应发挥重要作用。
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