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Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome
Herpes simplex virus type 1 (HSV-1) is a highly prevalent virus in humans and causes severe forms of inflammation, such as herpes simplex encephalitis (HSE). Pyroptosis is a new inflammatory cell death triggered by inflammasome and cysteine-requiring aspartate protease-1 (caspase-1) activation. None...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8978634/ https://www.ncbi.nlm.nih.gov/pubmed/35387080 http://dx.doi.org/10.3389/fmicb.2022.838808 |
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author | Hu, Xiao Zeng, Qiongzhen Xiao, Ji Qin, Shurong Wang, Yuan Shan, Tianhao Hu, Di Zhu, Yexuan Liu, Kaisheng Zheng, Kai Wang, Yifei Ren, Zhe |
author_facet | Hu, Xiao Zeng, Qiongzhen Xiao, Ji Qin, Shurong Wang, Yuan Shan, Tianhao Hu, Di Zhu, Yexuan Liu, Kaisheng Zheng, Kai Wang, Yifei Ren, Zhe |
author_sort | Hu, Xiao |
collection | PubMed |
description | Herpes simplex virus type 1 (HSV-1) is a highly prevalent virus in humans and causes severe forms of inflammation, such as herpes simplex encephalitis (HSE). Pyroptosis is a new inflammatory cell death triggered by inflammasome and cysteine-requiring aspartate protease-1 (caspase-1) activation. Nonetheless, HSV-1 induces encephalitis, and cell death mechanisms are not understood. In this study, we confirmed for the first time that the DNA virus HSV-1 triggers Gasdermin D-dependent pyroptosis by activating NLR family pyrin domain containing 3 (NLRP3) inflammasomes in mouse microglia, leading to mature IL-1β production and active caspase-1 (p10) release. Inhibition of microglial NLRP3 inflammasome activation suppressed HSV-1-induced Gasdermin D-dependent pyroptosis. In addition, NLRP3 and IL-1β expression levels were significantly increased in the mouse model of herpes simplex encephalitis compared with normal mice without viral infection. Collectively, our data revealed that the activation of inflammasomes and GSDMD-dependent pyroptosis is the mechanism of HSV-1 inducing inflammation and provides treatment targets for viral inflammation. |
format | Online Article Text |
id | pubmed-8978634 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-89786342022-04-05 Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome Hu, Xiao Zeng, Qiongzhen Xiao, Ji Qin, Shurong Wang, Yuan Shan, Tianhao Hu, Di Zhu, Yexuan Liu, Kaisheng Zheng, Kai Wang, Yifei Ren, Zhe Front Microbiol Microbiology Herpes simplex virus type 1 (HSV-1) is a highly prevalent virus in humans and causes severe forms of inflammation, such as herpes simplex encephalitis (HSE). Pyroptosis is a new inflammatory cell death triggered by inflammasome and cysteine-requiring aspartate protease-1 (caspase-1) activation. Nonetheless, HSV-1 induces encephalitis, and cell death mechanisms are not understood. In this study, we confirmed for the first time that the DNA virus HSV-1 triggers Gasdermin D-dependent pyroptosis by activating NLR family pyrin domain containing 3 (NLRP3) inflammasomes in mouse microglia, leading to mature IL-1β production and active caspase-1 (p10) release. Inhibition of microglial NLRP3 inflammasome activation suppressed HSV-1-induced Gasdermin D-dependent pyroptosis. In addition, NLRP3 and IL-1β expression levels were significantly increased in the mouse model of herpes simplex encephalitis compared with normal mice without viral infection. Collectively, our data revealed that the activation of inflammasomes and GSDMD-dependent pyroptosis is the mechanism of HSV-1 inducing inflammation and provides treatment targets for viral inflammation. Frontiers Media S.A. 2022-03-21 /pmc/articles/PMC8978634/ /pubmed/35387080 http://dx.doi.org/10.3389/fmicb.2022.838808 Text en Copyright © 2022 Hu, Zeng, Xiao, Qin, Wang, Shan, Hu, Zhu, Liu, Zheng, Wang and Ren. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Hu, Xiao Zeng, Qiongzhen Xiao, Ji Qin, Shurong Wang, Yuan Shan, Tianhao Hu, Di Zhu, Yexuan Liu, Kaisheng Zheng, Kai Wang, Yifei Ren, Zhe Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome |
title | Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome |
title_full | Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome |
title_fullStr | Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome |
title_full_unstemmed | Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome |
title_short | Herpes Simplex Virus 1 Induces Microglia Gasdermin D-Dependent Pyroptosis Through Activating the NLR Family Pyrin Domain Containing 3 Inflammasome |
title_sort | herpes simplex virus 1 induces microglia gasdermin d-dependent pyroptosis through activating the nlr family pyrin domain containing 3 inflammasome |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8978634/ https://www.ncbi.nlm.nih.gov/pubmed/35387080 http://dx.doi.org/10.3389/fmicb.2022.838808 |
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