PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue

Pseudorabies virus (PRV) can infect a wide range of animal species, including swine and rodents. Infection in pigs is associated with significant economic losses in the global pork industry and is characterized by acute, often fatal disease, as well as central nervous system (CNS) invasion, which le...

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Main Authors: Chunzi Peng, Jinwu Zhang, Changxu Wu, Danning Liu, Jing Liang, Maojie Lv, Shisen Yang, Xiaoning Li, Yingyi Wei, Hailan Chen, Jiakang He, Tingjun Hu, Meiling Yu
Format: Article
Language:English
Published: MDPI AG 2025-06-01
Series:Microorganisms
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Online Access:https://www.mdpi.com/2076-2607/13/7/1531
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author Chunzi Peng
Jinwu Zhang
Changxu Wu
Danning Liu
Jing Liang
Maojie Lv
Shisen Yang
Xiaoning Li
Yingyi Wei
Hailan Chen
Jiakang He
Tingjun Hu
Meiling Yu
author_facet Chunzi Peng
Jinwu Zhang
Changxu Wu
Danning Liu
Jing Liang
Maojie Lv
Shisen Yang
Xiaoning Li
Yingyi Wei
Hailan Chen
Jiakang He
Tingjun Hu
Meiling Yu
author_sort Chunzi Peng
collection DOAJ
description Pseudorabies virus (PRV) can infect a wide range of animal species, including swine and rodents. Infection in pigs is associated with significant economic losses in the global pork industry and is characterized by acute, often fatal disease, as well as central nervous system (CNS) invasion, which leads to neurological manifestations. Although PRV replication has been extensively characterized in certain murine neuronal cell lines such as Neuro-2a, the mechanisms underlying PRV-induced neuroinflammatory injury and necroptosis remain largely unclear. In this study, Kunming mice and mouse astrocytes (C8-D1A) were infected with PRV-GXLB-2013 at different doses to evaluate neurological injury and inflammatory responses. Given that the NF-κB/MLKL signaling pathway was found to be activated during PRV infection, a selective MLKL inhibitor, necrosulfonamide (NSA), was applied to investigate the role of necroptosis in PRV-induced neuroinflammatory damage. Mice infected with higher viral doses showed increased mortality, severe neurological symptoms, elevated brain inflammation, and pathological changes. In C8-D1A cells, PRV infection significantly upregulated inflammatory cytokines and key components of the NF-κB/MLKL pathway. Importantly, NSA treatment markedly reduced these inflammatory responses, mitochondrial damage, and cellular necrosis. Collectively, these findings suggest that PRV infection triggers neuroinflammatory injury through the activation of necroptosis and the NF-κB/MLKL signaling pathway. This study provides novel mechanistic insights into PRV-induced neurological damage and highlights potential therapeutic targets for intervention.
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spelling doaj-art-402b0598cf9246d89d43b9e989ddd9032025-08-20T02:47:09ZengMDPI AGMicroorganisms2076-26072025-06-01137153110.3390/microorganisms13071531PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain TissueChunzi Peng0Jinwu Zhang1Changxu Wu2Danning Liu3Jing Liang4Maojie Lv5Shisen Yang6Xiaoning Li7Yingyi Wei8Hailan Chen9Jiakang He10Tingjun Hu11Meiling Yu12Guangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaGuangxi Key Laboratory of Animal Breeding, Disease Control and Prevention, College of Animal Science and Technology, Guangxi University, Nanning 530004, ChinaPseudorabies virus (PRV) can infect a wide range of animal species, including swine and rodents. Infection in pigs is associated with significant economic losses in the global pork industry and is characterized by acute, often fatal disease, as well as central nervous system (CNS) invasion, which leads to neurological manifestations. Although PRV replication has been extensively characterized in certain murine neuronal cell lines such as Neuro-2a, the mechanisms underlying PRV-induced neuroinflammatory injury and necroptosis remain largely unclear. In this study, Kunming mice and mouse astrocytes (C8-D1A) were infected with PRV-GXLB-2013 at different doses to evaluate neurological injury and inflammatory responses. Given that the NF-κB/MLKL signaling pathway was found to be activated during PRV infection, a selective MLKL inhibitor, necrosulfonamide (NSA), was applied to investigate the role of necroptosis in PRV-induced neuroinflammatory damage. Mice infected with higher viral doses showed increased mortality, severe neurological symptoms, elevated brain inflammation, and pathological changes. In C8-D1A cells, PRV infection significantly upregulated inflammatory cytokines and key components of the NF-κB/MLKL pathway. Importantly, NSA treatment markedly reduced these inflammatory responses, mitochondrial damage, and cellular necrosis. Collectively, these findings suggest that PRV infection triggers neuroinflammatory injury through the activation of necroptosis and the NF-κB/MLKL signaling pathway. This study provides novel mechanistic insights into PRV-induced neurological damage and highlights potential therapeutic targets for intervention.https://www.mdpi.com/2076-2607/13/7/1531PRV infectionneurological inflammatory injurynecroptosisNF-κB signaling pathway
spellingShingle Chunzi Peng
Jinwu Zhang
Changxu Wu
Danning Liu
Jing Liang
Maojie Lv
Shisen Yang
Xiaoning Li
Yingyi Wei
Hailan Chen
Jiakang He
Tingjun Hu
Meiling Yu
PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue
Microorganisms
PRV infection
neurological inflammatory injury
necroptosis
NF-κB signaling pathway
title PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue
title_full PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue
title_fullStr PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue
title_full_unstemmed PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue
title_short PRV Induces Neurological Inflammatory Injury by Activating Necroptosis of Brain Tissue
title_sort prv induces neurological inflammatory injury by activating necroptosis of brain tissue
topic PRV infection
neurological inflammatory injury
necroptosis
NF-κB signaling pathway
url https://www.mdpi.com/2076-2607/13/7/1531
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