动物造模,感染免疫模型 z-bio 2022-09-01 409

　　Objective: Physiological aging leads to the down-regulation of the body's immune function, which in turn reduces the ability of the elderly to respond to infection, and increases the susceptibility to pathogens of emerging infectious diseases such as severe influenza virus. Therefore, this research group established an elderly mouse model fitted with clinical severe influenza virus infection to evaluate the immune response characteristics of elderly hosts.

　　METHODS: Aged C57 mice (18-24 months old) were infected with influenza virus H7N9 (high pathogenicity) and H9N2 (low pathogenicity) with different virulence respectively. The virus replication in the lung, the expression of inflammatory factors and the pathological damage of the lung were dynamically detected.

　　Results: Compared with the adult control mice (6-8 weeks old), the body weight of the aged mice decreased by 30% (the adult control only decreased by 10%) at 7 days after infection with H9N2, and the survival rate decreased to 50% (the adult control was 50%). 100%). The replication of H9N2 virus in the lungs of aged mice was higher (P<0.01), and peaked on the 2nd day after infection (3.2×104 RNA virus copies per gram of lungs). Lung inflammation represented by factor MCP-1 was overexpressed, which was 100-1000 times higher than that of adult controls; lung pathological staining indicated that the lung injury in aged mice was more serious, and the recovery time after infection was longer.

　　Conclusion: The infection model of aged mice was successfully established, which can reproduce the phenomenon of clinical infection immune response in terms of infection survival, lung virus replication and inflammatory damage. It can be used to deeply understand the mechanism of infection in aged hosts and evaluate anti-infective drugs.