• Penghui Yang, Hongjing Gu, Zhongpeng Zhao, Wei Wang, Bin Cao, Chengcai Lai, Xiaolan Yang, LiangYan Zhang, Yueqiang Duan, Shaogeng Zhang, Weiwen Chen, Wenbo Zhen, Maosheng Cai, Josef M Penninger, Chengyu Jiang, and Xiliang Wang.
• 1] State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing 100071, China [2] Beijing 302 Hospital, Beijing, 100039, China.
• Sci Rep. 2014 Nov 13; 4: 7027.

AbstractSince March 2013, the emergence of an avian-origin influenza A (H7N9) virus has raised concern in China. Although most infections resulted in respiratory illness, some severe cases resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that further contributes to morbidity. To date, no effective drugs that improve the clinical outcome of influenza A (H7N9) virus-infected patients have been identified. Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal disease, and acute lung injury. In the current study, we report that ACE2 could mediate the severe acute lung injury induced by influenza A (H7N9) virus infection in an experimental mouse model. Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor (AT1). The current findings demonstrate that ACE2 plays a critical role in influenza A (H7N9) virus-induced acute lung injury, and suggest that might be a useful potential therapeutic target for future influenza A (H7N9) outbreaks.

48 keywords...

hide…