Abstract: Objective
To establish a mouse model of influenza virus(IV) infection in haze environment, and to investigate its effect on the expression of tumor necrosis factor-α(TNF-α) in serum, airway secretory immunoglobulin A(sIgA) in nasopharyngeal lavage fluid and pulmonary surfactant-associated protein A(SP-A) in lung tissue of mice.
Methods
Seventy-two SPF grade BABL/c mice were randomly divided into the normal group (group A),PM2.5 tracheal drip group (group B),IV infection group(group C) and -PM2.5- tracheal drip+IV infection group(group D), with 18 rats in each group. Except the group A, the other groups of mice were treated with PM2.5 tracheal drip/IV infection model, and samples were obtained on the day of 3, 7, 10 after the model was established. The lung tissue sections were examined by histopathology; the serum levels of TNF-α and the nasopharyngeal lavage fluid sIgA in the mice were assessed by enzyme-linked immunosorbent assay(ELISA);the expression of SP-A protein in lung tissue of mice was detected by immunohistochemical SP method and Western-blot method.
Results
After double infection with PM2.5 and IV in mice, the pathological examination revealed thickening of alveolar septum and bronchioles, and extensive inflammatory cell infiltration in the lung tissues; the expression of TNF-α in serum of mice was significantly up-regulated; the content of sIgA in nasopharyngeal lavage fluid and the expression of SP-A in lungs of mice decreased. Compared with group B, group C could decrease the expression of sIgA in nasopharyngeal lavage fluid and SP-A in lung, and there was no significant difference at each time point(P>0.05);the expression of sIgA and SP-A was significantly decreased in group D on day 3 and 7(P<0.05),and it began to rise gradually on the tenth day.
Conclusion
In this experiment, all three methods of modeling have caused lung injury in varying degrees; especially, the lung injury caused by PM2.5 tracheal drip and IV infection is the most serious. Therefore, it is proved that this method is simple and reliable, which is helpful for further study of pulmonary diseases and inflammation mechanism.

Key words: Haze, PM2.5, Modeling, Influenza virus, Immune injury