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为研究H9N2亚型禽流感病毒(H9N2 AIV)继发细菌感染的作用机制,以BALB/c小鼠为模型,研究呼吸道感染H9N2 AIV后,宿主肠道菌群结构、黏膜屏障、黏膜炎症反应等情况。结果显示:H9N2 AIV经呼吸道感染BALB/c小鼠后,小鼠肠道菌群紊乱。攻毒后小鼠体内的葡萄球菌属、链球菌属和棒状杆菌属极显著增加(P<0.01),而有益菌为主的乳杆菌属等极显著降低(P<0.01);H9N2 AIV感染小鼠后,肠道黏膜屏障被破坏,促炎因子IFN-γ、IFN-β等极显著高表达(P<0.01),上皮细胞中的ZO-1等紧密连接蛋白则明显下调(P<0.05),造成肠壁通透性增强。研究表明小鼠感染H9N2 AIV后,其肠道微生物菌群失衡、黏膜屏障功能被破坏、出现炎症反应等。
In order to study the mechanism of bacterial infection secondary to H9N2 AIV, BALB / c mice were used to study the intestinal flora, mucosal barrier and mucosal inflammatory response after H9N2 AIV infection Happening. The results showed that: intestinal flora of mice was disturbed after H9N2 AIV was infected by respiratory tract in BALB / c mice. Staphylococcus, Streptococcus and Corynebacterium were significantly increased (P <0.01), while those with beneficial bacteria were significantly decreased (P <0.01). H9N2 AIV infection was small The intestinal mucosal barrier was destroyed, the expression of proinflammatory cytokines such as IFN-γ and IFN-β were significantly increased (P <0.01), while the tight junction proteins such as ZO-1 in epithelial cells were significantly decreased , Resulting in increased permeability of the intestinal wall. Studies have shown that mice infected with H9N2 AIV, the intestinal microflora imbalance in the flora, mucosal barrier function is destroyed, the inflammatory response.