Objective: Physiological aging leads to the down-regulation of the immune function of the body, which in turn reduces the immune response to infection in the elderly, and increases the susceptibility to new and sudden infectious diseases such as severe influenza virus. After the infection, the clinical symptoms are more serious and the prognosis Poor. Therefore, our research group established a clinical model of severe influenza virus infection in elderly mice to evaluate the immune response characteristics of elderly host infections.
Methods: Influenza virus H7N9 (high pathogenicity) and H9N2 (low pathogenicity) of different virulence were used to infect elderly C57 mice (18~24 months old) by intranasal drip, and their weight changes and survival conditions after infection were analyzed. And dynamically detect the replication of the virus in the lung, the expression of inflammatory factors and the pathological damage of the lung.
Results: Compared with adult control mice (6 to 8 weeks old), the body weight of elderly mice was reduced by 30% (the adult control only decreased by 10%) and the survival rate was reduced to 50% (the adult control was 100%). The H9N2 virus replication in the lungs of old mice is higher (P<0.01), reaching a peak on the second day after infection (3.2×104 copies of RNA virus in the lungs per gram); inflammatory factor IL-6, chemotaxis The overexpression of inflammation in the lung represented by factor MCP-1 is 100-1000 times that of adult controls; lung pathological staining indicates that the lung injury in elderly mice is more serious, and the repair time after infection is longer.
Conclusion: The successful establishment of an old mouse infection model can reproduce the clinical infection immune response in terms of infection survival, lung virus replication and inflammatory damage. It can be used to deeply understand the mechanism research related to the elderly host infection and the evaluation of anti-infective drugs.