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Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion

Zika virus (ZIKV) infection is a public health emergency and host innate immunity is essential for the control of virus infection. The NLRP3 inflammasome plays a key role in host innate immune responses by activating caspase-1 to facilitate interleukin-1β (IL-1β) secretion. Here we report that ZIKV...

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Autores principales: Wang, Wenbiao, Li, Geng, De Wu, Luo, Zhen, Pan, Pan, Tian, Mingfu, Wang, Yingchong, Xiao, Feng, Li, Aixin, Wu, Kailang, Liu, Xiaohong, Rao, Lang, Liu, Fang, Liu, Yingle, Wu, Jianguo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5760693/
https://www.ncbi.nlm.nih.gov/pubmed/29317641
http://dx.doi.org/10.1038/s41467-017-02645-3
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author Wang, Wenbiao
Li, Geng
De Wu
Luo, Zhen
Pan, Pan
Tian, Mingfu
Wang, Yingchong
Xiao, Feng
Li, Aixin
Wu, Kailang
Liu, Xiaohong
Rao, Lang
Liu, Fang
Liu, Yingle
Wu, Jianguo
author_facet Wang, Wenbiao
Li, Geng
De Wu
Luo, Zhen
Pan, Pan
Tian, Mingfu
Wang, Yingchong
Xiao, Feng
Li, Aixin
Wu, Kailang
Liu, Xiaohong
Rao, Lang
Liu, Fang
Liu, Yingle
Wu, Jianguo
author_sort Wang, Wenbiao
collection PubMed
description Zika virus (ZIKV) infection is a public health emergency and host innate immunity is essential for the control of virus infection. The NLRP3 inflammasome plays a key role in host innate immune responses by activating caspase-1 to facilitate interleukin-1β (IL-1β) secretion. Here we report that ZIKV stimulates IL-1β secretion in infected patients, human PBMCs and macrophages, mice, and mice BMDCs. The knockdown of NLRP3 in cells and knockout of NLRP3 in mice inhibit ZIKV-mediated IL-1β secretion, indicating an essential role for NLRP3 in ZIKV-induced IL-1β activation. Moreover, ZIKV NS5 protein is required for NLRP3 activation and IL-1β secretion by binding with NLRP3 to facilitate the inflammasome complex assembly. Finally, ZIKV infection in mice activates IL-1β secretion, leading to inflammatory responses in the mice brain, spleen, liver, and kidney. Thus we reveal a mechanism by which ZIKV induces inflammatory responses by facilitating NLRP3 inflammasome complex assembly and IL-1β activation.
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spelling pubmed-57606932018-01-12 Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion Wang, Wenbiao Li, Geng De Wu Luo, Zhen Pan, Pan Tian, Mingfu Wang, Yingchong Xiao, Feng Li, Aixin Wu, Kailang Liu, Xiaohong Rao, Lang Liu, Fang Liu, Yingle Wu, Jianguo Nat Commun Article Zika virus (ZIKV) infection is a public health emergency and host innate immunity is essential for the control of virus infection. The NLRP3 inflammasome plays a key role in host innate immune responses by activating caspase-1 to facilitate interleukin-1β (IL-1β) secretion. Here we report that ZIKV stimulates IL-1β secretion in infected patients, human PBMCs and macrophages, mice, and mice BMDCs. The knockdown of NLRP3 in cells and knockout of NLRP3 in mice inhibit ZIKV-mediated IL-1β secretion, indicating an essential role for NLRP3 in ZIKV-induced IL-1β activation. Moreover, ZIKV NS5 protein is required for NLRP3 activation and IL-1β secretion by binding with NLRP3 to facilitate the inflammasome complex assembly. Finally, ZIKV infection in mice activates IL-1β secretion, leading to inflammatory responses in the mice brain, spleen, liver, and kidney. Thus we reveal a mechanism by which ZIKV induces inflammatory responses by facilitating NLRP3 inflammasome complex assembly and IL-1β activation. Nature Publishing Group UK 2018-01-09 /pmc/articles/PMC5760693/ /pubmed/29317641 http://dx.doi.org/10.1038/s41467-017-02645-3 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Wang, Wenbiao
Li, Geng
De Wu
Luo, Zhen
Pan, Pan
Tian, Mingfu
Wang, Yingchong
Xiao, Feng
Li, Aixin
Wu, Kailang
Liu, Xiaohong
Rao, Lang
Liu, Fang
Liu, Yingle
Wu, Jianguo
Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion
title Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion
title_full Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion
title_fullStr Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion
title_full_unstemmed Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion
title_short Zika virus infection induces host inflammatory responses by facilitating NLRP3 inflammasome assembly and interleukin-1β secretion
title_sort zika virus infection induces host inflammatory responses by facilitating nlrp3 inflammasome assembly and interleukin-1β secretion
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5760693/
https://www.ncbi.nlm.nih.gov/pubmed/29317641
http://dx.doi.org/10.1038/s41467-017-02645-3
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