Research Papers: Immunology:
RIP3 deficiency ameliorates inflammatory response in mice infected with influenza H7N9 virus infection
Metrics: PDF 1746 views | HTML 2867 views | ?
Yu-Lin Xu1,*, Hai-Lin Tang1,*, Hao-Ran Peng1, Ping Zhao1, Zhong-Tian Qi1 and Wen Wang1
1 Department of Microbiology, Shanghai Key Laboratory of Medical Biodefense, Second Military Medical University, Shanghai, China
* These authors have contributed equally to this study
Zhong-Tian Qi, email:
Wen Wang, email:
Keywords: influenza A virus; H7N9 virus; RIP3; necroptosis; proinflammatory cytokines; Immunology and Microbiology Section; Immune response; Immunity
Received: December 08, 2016 Accepted: February 23, 2017 Published: March 08, 2017
Influenza H7N9 virus infection causes an acute, highly contagious respiratory illness that triggers cell death of infected cells and airway epithelial destruction. RIP3 is a key regulator of cell death responses to a growing number of viral and microbial agents. This study aimed to investigate the role of RIP3 in inflammation of influenza H7N9 virus infection. Here, RIP3 knock out (RIP3-/-) mice and littermate wild type mice were infected intranasally with influenza H7N9 virus (A/Fujian/S03/2015) to determine the contribution of RIP3 to the inflammatory response of influenza H7N9 virus infection. It was found that RIP3-/- mice infected with H7N9 virus showed higher survival and less weight loss, compared with wild type littermate mice. In addition, RIP3-/- mice had fewer regions of edema, infiltration with inflammatory cells, and alveolar collapses, and the secretions of IL-1β, IL-6, RANTES and MIP-1 in BALF were significantly decreased on days 3 and 7 p.i. when compared with WT mice. Moreover, caspase 1/IL1β signaling was found to be involved in RIP3 associated inflammation of influenza H7N9 virus, but not RIP3/MLKL dependent necrosis. In the conclusion, our results indicated that RIP3 deficiency can protect mice from the infection of influenza H7N9 virus by downregulating caspase 1/IL1β signaling, which provided evidence of the RIP3 involved necroptosis independent manner.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.