Wu Sha, Yan Yuqi, Zhang Mengyuan, Shi Shanshan, Jiang Zhenyou
Department of Microbiology and Immunology, School of Medicine, Jinan University, Guangzhou 510632, China.
Department of Microbiology and Immunology, School of Medicine, Jinan University, Guangzhou 510632, China. *Corresponding authors, E-mail:
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2016 Apr;32(4):433-6, 441.
To investigate the relationship between the intestinal disorder of anaerobic bacteria and influenza virus infection, and the effect on pulmonary inflammatory cytokines in mice.
Totally 36 mice were randomly divided into normal control group, virus-infected group and metronidazole treatment group (12 mice in each group). Mice in the metronidazole group were administrated orally with metronidazole sulfate for 8 days causing anaerobic bacteria flora imbalance; then all groups except the normal control group were treated transnasally with influenza virus (50 μL/d FM1) for 4 days to establish the influenza virus-infected models. Their mental state and lung index were observed, and the pathological morphological changes of lung tissues, caecum and intestinal mucosa were examined by HE staining. The levels of interleukin 4 (IL-4), interferon γ (IFN-γ), IL-10 and IL-17 in the lung homogenates were determined by ELISA.
Compared with the virus control group, the metronidazole group showed obviously increased lung index and more serious pathological changes of the lung tissue and appendix inflammation performance. After infected by the FM1 influenza virus, IFN-γ and IL-17 of the metronidazole group decreased significantly and IL-4 and IL-10 levels were raised, but there was no statistically difference between the metronidazole and virus control groups.
Intestinal anaerobic bacteria may inhibit the adaptive immune response in the lungs of mice infected with FM1 influenza virus through adjusting the lung inflammatory factors, affect the replication and clean-up time of the FM1 influenza virus, thus further aggravating pulmonary immune pathological injury caused by the influenza virus infection.
探讨厌氧菌肠道紊乱与流感病毒感染之间的关系,以及对小鼠肺炎性细胞因子的影响。
将36只小鼠随机分为正常对照组、病毒感染组和甲硝唑治疗组(每组12只)。甲硝唑组小鼠口服硫酸甲硝唑8天致厌氧菌菌群失调;然后除正常对照组外,其余各组经鼻给予流感病毒(50 μL/d FM1)处理4天以建立流感病毒感染模型。观察其精神状态和肺指数,通过HE染色检查肺组织、盲肠和肠黏膜的病理形态变化。采用ELISA法测定肺匀浆中白细胞介素4(IL-4)、干扰素γ(IFN-γ)、IL-10和IL-17的水平。
与病毒对照组相比,甲硝唑组肺指数明显升高,肺组织病理变化及阑尾炎症表现更严重。FM1流感病毒感染后,甲硝唑组IFN-γ和IL-17显著降低,IL-4和IL-10水平升高,但甲硝唑组与病毒对照组之间无统计学差异。
肠道厌氧菌可能通过调节肺部炎性因子抑制感染FM1流感病毒小鼠肺部的适应性免疫反应,影响FM1流感病毒的复制和清除时间,从而进一步加重流感病毒感染所致的肺部免疫病理损伤。