RESUMO
Objective To investigate the mechanism of pulmonary inflammation induced by influenza virus , and provide reference for the development of effective drugs for viral pneumonia .Methods An influenza PR8 infection mouse model was established .The levels of inflammatory cytokines and complement molecules were determined using RT -PCR and ELISA.The pathological changes were examined using biopsy .The complement inhibitor cobra venom factor ( CVF) was injected intraperitoneally at a dose of 50 μg/( kg· 24 h) , and then body mass .The survival rate and inflammatory factors were examined .Results Compared with the control group , the expressions of complement regulatory molecule Crry and CD59 were significantly decreased (P<0.01), while those of complement C9 and complement receptor C3aR and C5aR were significantly increased in the lungs of influenza model mice (P<0.01).Pro-inflammatory cytokines TNF-α, IL-6 and IFN-γwere highly expressed , but anti-inflammatory cytokine IL-2 was lowly expressed in serum .Treatment with CVF caused a sight body mass loss, a survival rate increase and a lung index decrease (P <0.05).Moreover, an IL-2 expression increase and a decrease of IL-6, TNF -αand INF-γexpression were observed in CVF treatment mice ( P< 0.05).Conclusion Inhibition of complement activation can increase the survival rate of mice with influenza pneumonia and decrease pulmonary indexes .thus delaying the pathogenesis of PR 8.
