The immunological mechanisms of secondary bacterial infection followed by influenza virus infection were examined. When mice were intranasally infected with influenza virus A and then infected with P. aeruginosa at 4 days after viral infection, bacterial clearance in the lung significantly decreased compared to that of non-viral infected mice. Neutrophils from viral infected mice showed impaired digestion and/or killing of phagocytized bacteria due to reduced myeloperoxidase (MPO) activity. G-CSF production in the lungs of viral infected mice was lower than that of non-viral infected mice after secondary bacterial infection. When viral infected mice were injected with G-CSF before secondary bacterial infection, the MPO activity of viral infected mice restored to the same level as that of non-infected mice. Bacteria clearance in viral infected mice was also recovered by G-CSF administration. Thus, neutrophil dysfunction caused by influenza virus is attributed to insufficient G-CSF production, which induces a secondary bacterial infection.
Ishikawa, H., Fukui, T., Ino, S., Sasaki, H., Awano, N., Kohda, C., & Tanaka, K. (2016). Influenza virus infection causes neutrophil dysfunction through reduced G-CSF production and an increased risk of secondary bacteria infection in the lung. Virology, 499, 23–29. https://doi.org/10.1016/j.virol.2016.08.025