Cargando…
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...
Autores principales: | , , , , , , , , , , , , , , |
---|---|
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 |
_version_ | 1783291412433862656 |
---|---|
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. |
format | Online Article Text |
id | pubmed-5760693 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT wangwenbiao zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT ligeng zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT dewu zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT luozhen zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT panpan zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT tianmingfu zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT wangyingchong zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT xiaofeng zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT liaixin zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT wukailang zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT liuxiaohong zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT raolang zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT liufang zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT liuyingle zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion AT wujianguo zikavirusinfectioninduceshostinflammatoryresponsesbyfacilitatingnlrp3inflammasomeassemblyandinterleukin1bsecretion |