Newcastle disease virus infection induces activation of the NLRP3 inflammasome

Abstract 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 hairp...

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Veröffentlicht in:Virology (New York, N.Y.) N.Y.), 2016-09, Vol.496, p.90-96
Hauptverfasser: Wang, Binbin, Zhu, Jie, Li, Dandan, Wang, Yang, Zhan, Yuan, Tan, Lei, Qiu, Xusheng, Sun, Yingjie, Song, Cuiping, Meng, Chunchun, Ying, Liao, Xiang, Mao, Meng, Guangxun, Ding, Chan
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container_start_page 90
container_title Virology (New York, N.Y.)
container_volume 496
creator Wang, Binbin
Zhu, Jie
Li, Dandan
Wang, Yang
Zhan, Yuan
Tan, Lei
Qiu, Xusheng
Sun, Yingjie
Song, Cuiping
Meng, Chunchun
Ying, Liao
Xiang, Mao
Meng, Guangxun
Ding, Chan
description Abstract 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.
doi_str_mv 10.1016/j.virol.2016.05.023
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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. 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subjects Animals
Caspase 1 - metabolism
Caspase Inhibitors - pharmacology
Caspase-1
Cell Line
Disease Models, Animal
Female
Humans
Infectious Disease
Inflammasome
Inflammasomes - metabolism
Interleukin-1beta - biosynthesis
Macrophage Activation - immunology
Macrophages - immunology
Macrophages - metabolism
Macrophages - virology
Mice
Mice, Knockout
NDV
Newcastle Disease - genetics
Newcastle Disease - metabolism
Newcastle Disease - virology
Newcastle disease virus - physiology
NLR Family, Pyrin Domain-Containing 3 Protein - genetics
NLR Family, Pyrin Domain-Containing 3 Protein - metabolism
NLRP3
THP‐1 cells
Virus Replication
title Newcastle disease virus infection induces activation of the NLRP3 inflammasome
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