Intranasal application of polyethyleneimine suppresses influenza virus infection in mice

He, Biao; Fu, Yuhong; Xia, Shuai; Yu, Fei; Wang, Qian; Lu, Lu; Jiang, Shibo

To elucidate the mechanism of action of PEI, we examined the RNA levels of IFN-α4, IFN-β, IFN-γ, GM-CSF, IFITM3 and IL-17 in the lungs of mice pretreated with PEI, CTB, and PBS, respectively, before viral challenge using quantitative reverse transcription-PCR (qRT-PCR). As previously reported, some of these cytokines, such as interferon, GM-CSF and IFITM3, were effective in protecting against influenza infection. [6] [7] [8] As shown in Supplementary Figure S1 , PEI induced a significantly higher RNA level of IFN-α4 than CTB or PBS. Furthermore, the RNA levels of GM-CSF and IFITM3 elicited by PEI were similar to those induced by CTB but much higher than those induced by PBS. The RNA level of IL-17 in mice pretreated with CTB, an IL-17-inducing adjuvant, was approximately 7-and 42-fold higher than that in mice pretreated with PEI and PBS, respectively. These results suggest that IFN-α4, GM-CSF, and IFITM3 are 'good cytokines' because they act as protective mediators against influenza virus infection, whereas IL-17 is a 'bad cytokine' that exacerbates pathology, primarily in the lung, after influenza infection.