Pulmonary immune responses to 2009 pandemic influenza A (H1N1) virus in mice
- Equal contributors
1 The Second Artillery General Hospital, PLA, Beijing 100088, China
2 State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, 20 Dong-Da Street, Fengtai District, Beijing 100071, P.R. China
3 Department of Biochemistry, the University of Hong Kong, Pokfulam, Hong Kong, China
4 Cellular Technology Ltd, No.1 Qijie, Road Shangdi, Haidian District, Beijing 100085, China
BMC Infectious Diseases 2014, 14:197 doi:10.1186/1471-2334-14-197Published: 12 April 2014
Well-characterized mice models will afford a cheaper, easy-handling opportunity for a more comprehensive understanding of 2009 influenza A (H1N1) virus’s pathogenesis potential. We aimed to provide a robust description of pulmonary immune responses in the mice infected by the virus.
BALB/c mice were inoculated intranasally with A/Beijing/501/2009(H1N1) (BJ501) and A/PR/8/34(H1N1) (PR8) viruses and compared for survival rate, viral replication, and kinetics of pulmonary immune responses.
BJ501 virus replicated less efficiently in the lungs than PR8, and both caused lethal illness in the mice. The transient increases of pulmonary TNF-α 2 days post infection for BJ501 and of INF-γ and IL-10 at 6 days post infection for PR8 were observed. IL-2+ and IL-4+ secreting cells showed significant increase 12 days post infection, while IFN-γ+, IgG+ and IgA+ secreting cells increased 6 days post infection. The different patterns of pulmonary immunological parameters between two viruses were at most seen in IL-6, IL-17 secretion and IgG1/IgG2a ratio.
The BALB/c mouse is evaluated as a good pathogenic model for studying BJ501 2009 H1N1 virus. The work provided some basic and detailed data, which might be referred when further evaluating innate and adapted pulmonary immune responses and local viral load in mice.