Newcastle disease virus infection induces activation of the NLRP3 inflammasome.
Inflammatory responses are important aspects of the innate immune system during virus infection. We found that Newcastle disease virus can induce inflammasome activation in the human macrophage-like cell line THP-1. Viral replication was required for inflammasome activation, and small hairpin RNA knockdown experiments indicated that IL-1β secretion was mediated by the NLRP3 inflammasome. We also verified the results in LPS-primed bone marrow-derived macrophages (BMDMs) from NLRP3-deficient and wild type mice. NDV is considered to be a promising oncolytic virus. Stimulating the immune system has been proposed as a key mechanism of oncolytic specificity, and the inflammasome appears to be an important mechanism by which NDV is controlled. Knockdown of inflammasome components or chemical inhibition of caspase-1 activity shows that cell survival was augmented and benefited NDV replication. This study shows that NLRP3 inflammasome activation is an innate cellular response to NDV infection and offers insights into the oncolytic specificity of NDV.
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Binbin
B
Wang
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Jie
J
Zhu
College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi 712100, China.
Dandan
D
Li
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Yang
Y
Wang
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Yuan
Y
Zhan
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Lei
L
Tan
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Xusheng
X
Qiu
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Yingjie
Y
Sun
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Cuiping
C
Song
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Chunchun
C
Meng
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Liao
L
Ying
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China.
Mao
M
Xiang
Unit of Innate Immunity, Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Guangxun
G
Meng
Shanghai Veterinary Research Institute, CAAS, Shanghai 200241, China. Electronic address: shoveldeen@shvri.ac.cn.
Chan
C
Ding
D000818:Animals; D020170:Caspase 1 / Q000378:metabolism; D061945:Caspase Inhibitors / Q000494:pharmacology; D002460:Cell Line; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism*; D053583:Interleukin-1beta / Q000096:biosynthesis; D008262:Macrophage Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000821:virology; D051379:Mice; D018345:Mice, Knockout; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000235:genetics / Q000378:metabolism*; D009521:Newcastle Disease / Q000235:genetics / Q000378:metabolism* / Q000821:virology*; D009522:Newcastle disease virus / Q000502:physiology*; D014779:Virus Replication
D061945:Caspase Inhibitors; D058847:Inflammasomes; D053583:Interleukin-1beta; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D020170:Caspase 1
Caspase-1; Inflammasome; NDV; NLRP3; THP‐1 cells