title: [Intestinal disorder of anaerobic bacteria aggravates pulmonary immune pathological injury of mice infected with influenza virus].
abstract: OBJECTIVE
  To investigate the relationship between the intestinal disorder of anaerobic bacteria and influenza virus infection, and the effect on pulmonary inflammatory cytokines in mice.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Microbiology and Immunology, School of Medicine, Jinan University, Guangzhou 510632, China.
authors.forename: Sha
authors.initials: S
authors.lastname: Wu
authors.affiliation: Department of Microbiology and Immunology, School of Medicine, Jinan University, Guangzhou 510632, China.
authors.forename: Yuqi
authors.initials: Y
authors.lastname: Yan
authors.affiliation: Department of Microbiology and Immunology, School of Medicine, Jinan University, Guangzhou 510632, China.
authors.forename: Mengyuan
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Department of Microbiology and Immunology, School of Medicine, Jinan University, Guangzhou 510632, China.
authors.forename: Shanshan
authors.initials: S
authors.lastname: Shi
authors.affiliation: Department of Microbiology and Immunology, School of Medicine, Jinan University, Guangzhou 510632, China. *Corresponding authors, E-mail: tjzhy@jnu.edu.cn.
authors.forename: Zhenyou
authors.initials: Z
authors.lastname: Jiang
mesh_terms: D000818:Animals; D001421:Bacteria, Anaerobic / Q000502:physiology*; D004195:Disease Models, Animal; D005260:Female; D000069196:Gastrointestinal Microbiome; D006801:Humans; D007251:Influenza, Human / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000821:virology*; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology; D007422:Intestines / Q000276:immunology / Q000382:microbiology*; D008168:Lung / Q000276:immunology* / Q000473:pathology / Q000821:virology; D051379:Mice; D008807:Mice, Inbred BALB C; D009975:Orthomyxoviridae / Q000502:physiology*
chemical_list: D020381:Interleukin-17; D016753:Interleukin-10; D007371:Interferon-gamma