Journal Article

IL-17 response mediates acute lung injury induced by the 2009 Pandemic Influenza A （HIN1） Virus

Chenggang Li Penghui Yang Yang Sun Taisheng Li Chen Wang Zhong Wang Zhen Zou Yiwu Yan Wei Wang Chen Wang Zhongwei Chen Li Xing Chong Tang Xiangwu Ju Feng Guo Jiejie Deng Yan Zhao Peng Yang Jun Tang Huanling Wang Zhongpeng Zhao Zhinan Yin Bin Cao Xiliang Wang Chengyu Jiang

2012

Overview

The 2009 flu pandemic involved the emergence of a new strain of a swine-origin H1N1 influenza virus （S-OIV H1N1） that infected almost every country in the world. Most infections resulted in respiratory illness and some severe cases resulted in acute lung injury. In this report, we are the first to describe a mouse model of S-OIV virus infection with acute lung injury and immune responses that reflect human clinical disease. The clinical efficacy of the antiviral oseltamivir （Tamiflu） administered in the early stages of S-OIV H1N1 infection was confirmed in the mouse model. Moreover, elevated levels of IL-17, Th-17 mediators and IL-17-responsive cytokines were found in serum samples of S-OIV-infected patients in Beijing. IL-17 deficiency or treatment with monoclonal antibodies against IL- 17-ameliorated acute lung injury induced by the S-OIV HIN1 virus in mice. These results suggest that IL-17 plays an important role in S-OIV-induced acute lung injury and that monoclonal antibodies against IL-17 could be useful as a potential therapeutic remedy for future S-OIV H1N1 pandemics.

• Subject: A型流感病毒 / IL-17 / 介导 / 免疫反应 / 单克隆抗体 / 急性肺损伤 / 病毒感染 / 诱导