NDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathway

Abstract Newcastle disease (ND), caused by the Newcastle disease virus (NDV), is a highly virulent infectious disease of poultry. Virulent NDV can cause severe autophagy and inflammation in host cells. While studies have shown a mutual regulatory relationship between autophagy and inflammation, this...

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Main Authors: Juncheng Cai, Siyuan Wang, Haoyun Du, Lei Fan, WeiFeng Yuan, Qiufan Xu, Jinlian Ren, Qiuyan Lin, Bin Xiang, Chan Ding, Tao Ren, Libin Chen
Format: Article
Language:English
Published: BMC 2023-06-01
Series:Veterinary Research
Subjects:
Online Access:https://doi.org/10.1186/s13567-023-01174-w
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author Juncheng Cai
Siyuan Wang
Haoyun Du
Lei Fan
WeiFeng Yuan
Qiufan Xu
Jinlian Ren
Qiuyan Lin
Bin Xiang
Chan Ding
Tao Ren
Libin Chen
author_facet Juncheng Cai
Siyuan Wang
Haoyun Du
Lei Fan
WeiFeng Yuan
Qiufan Xu
Jinlian Ren
Qiuyan Lin
Bin Xiang
Chan Ding
Tao Ren
Libin Chen
author_sort Juncheng Cai
collection DOAJ
description Abstract Newcastle disease (ND), caused by the Newcastle disease virus (NDV), is a highly virulent infectious disease of poultry. Virulent NDV can cause severe autophagy and inflammation in host cells. While studies have shown a mutual regulatory relationship between autophagy and inflammation, this relationship in NDV infection remains unclear. This study confirmed that NDV infection could trigger autophagy in DF-1 cells to promote cytopathic and viral replication. NDV-induced autophagy was positively correlated with the mRNA levels of inflammatory cytokines such as IL-1β, IL-8, IL-18, CCL-5, and TNF-α, suggesting that NDV-induced autophagy promotes the expression of inflammatory cytokines. Further investigation demonstrated that NLRP3 protein expression, Caspase-1 activity, and p38 phosphorylation level positively correlated with autophagy, suggesting that NDV-induced autophagy could promote the expression of inflammatory cytokines through NLRP3/Caspase-1 inflammasomes and p38/MAPK pathway. In addition, NDV infection also triggered mitochondrial damage and mitophagy in DF-1 cells, but did not result in a large leakage of reactive oxygen species (ROS) and mitochondrial DNA (mtDNA), indicating that mitochondrial damage and mitophagy do not contribute to the inflammation response during NDV infection.
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spelling doaj.art-ef7879618c05495ead8e076d47bb950e2023-06-11T11:22:31ZengBMCVeterinary Research1297-97162023-06-0154111510.1186/s13567-023-01174-wNDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathwayJuncheng Cai0Siyuan Wang1Haoyun Du2Lei Fan3WeiFeng Yuan4Qiufan Xu5Jinlian Ren6Qiuyan Lin7Bin Xiang8Chan Ding9Tao Ren10Libin Chen11College of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, Yunnan Agricultural UniversityShanghai Veterinary Research Institute, Chinese Academy of Agricultural SciencesCollege of Veterinary Medicine, South China Agricultural UniversityCollege of Veterinary Medicine, South China Agricultural UniversityAbstract Newcastle disease (ND), caused by the Newcastle disease virus (NDV), is a highly virulent infectious disease of poultry. Virulent NDV can cause severe autophagy and inflammation in host cells. While studies have shown a mutual regulatory relationship between autophagy and inflammation, this relationship in NDV infection remains unclear. This study confirmed that NDV infection could trigger autophagy in DF-1 cells to promote cytopathic and viral replication. NDV-induced autophagy was positively correlated with the mRNA levels of inflammatory cytokines such as IL-1β, IL-8, IL-18, CCL-5, and TNF-α, suggesting that NDV-induced autophagy promotes the expression of inflammatory cytokines. Further investigation demonstrated that NLRP3 protein expression, Caspase-1 activity, and p38 phosphorylation level positively correlated with autophagy, suggesting that NDV-induced autophagy could promote the expression of inflammatory cytokines through NLRP3/Caspase-1 inflammasomes and p38/MAPK pathway. In addition, NDV infection also triggered mitochondrial damage and mitophagy in DF-1 cells, but did not result in a large leakage of reactive oxygen species (ROS) and mitochondrial DNA (mtDNA), indicating that mitochondrial damage and mitophagy do not contribute to the inflammation response during NDV infection.https://doi.org/10.1186/s13567-023-01174-wAutophagyinflammationmitochondrial damagemitophagyNewcastle disease virus
spellingShingle Juncheng Cai
Siyuan Wang
Haoyun Du
Lei Fan
WeiFeng Yuan
Qiufan Xu
Jinlian Ren
Qiuyan Lin
Bin Xiang
Chan Ding
Tao Ren
Libin Chen
NDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathway
Veterinary Research
Autophagy
inflammation
mitochondrial damage
mitophagy
Newcastle disease virus
title NDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathway
title_full NDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathway
title_fullStr NDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathway
title_full_unstemmed NDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathway
title_short NDV-induced autophagy enhances inflammation through NLRP3/Caspase-1 inflammasomes and the p38/MAPK pathway
title_sort ndv induced autophagy enhances inflammation through nlrp3 caspase 1 inflammasomes and the p38 mapk pathway
topic Autophagy
inflammation
mitochondrial damage
mitophagy
Newcastle disease virus
url https://doi.org/10.1186/s13567-023-01174-w
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