Hongtao Chen , Shihui Zhao , Shanling Liu , Yiming Wei , Yanbing Guo , Kun Gao , Hongze Shao , Han Zhao , Di Bao , Shuang Zhang , Shushuai Yi , Kai Wang , Guixue Hu
{"title":"FCV通过离子依赖途径激活NLRP3炎性体,促进IL-1β分泌","authors":"Hongtao Chen , Shihui Zhao , Shanling Liu , Yiming Wei , Yanbing Guo , Kun Gao , Hongze Shao , Han Zhao , Di Bao , Shuang Zhang , Shushuai Yi , Kai Wang , Guixue Hu","doi":"10.1016/j.vetmic.2025.110628","DOIUrl":null,"url":null,"abstract":"<div><div>Feline calicivirus (FCV) poses a significant threat to the health of susceptible animals in the global epidemic. The inflammasome plays a crucial role in the inflammatory process induced by pathogens, functioning in resisting their invasion, responding to cellular damage, and maintaining internal environmental homeostasis.FCV infection in cats causes inflammation,and the regulatory mecha-nisms of the NLRP3 inflammasome on inflammatory factors in infected cells urgently require further investigation.This study focuses on this inflammasome as the entry point, focusing on its activation signal that activates IL-1β secretion.Through cellular experiments, it analyzes the molecular mechanisms and logical relationships between this inflammasome, intracellular environ-ment, pyroptosis, the regulation of IL-1β secretion by viral-encoded proteins.The results showed that FCV-infected cells induced the activation and assembly of the NLRP3 inflammasome, thereby activating this signaling. FCV-induced IL-1β secretion was dependent on the activation of this inflammasome. In the early stages of infection, the activation of this inflammasome and IL-1β secretion were dependent on cellular Ca<sup>2 +</sup> influx and K<sup>+</sup> efflux. IL-1β secretion also relied on FCV-induced pyroptosis;The activation of this inflammasome by the FCV-encoded protein p32/LC and the subsequent induction of IL-1β secretion are contingent upon the function of its in mediating cellular Ca<sup>2+</sup> influx and K<sup>+</sup> efflux.In summary, this study demonstrates that following FCV infection of cells, its p32 and LC proteins activate the NLRP3 inflammasome activation signal in a manner dependent on Ca<sup>2+</sup> influx and K<sup>+</sup> efflux,Induce IL-1β secretion. In addition, FCV-induced pyroptosis also triggers the secretion of IL-1β. The findings of this study elucidate the leading to inflammatory mechanisms of FCV from a novel perspective, providing new drug targets for the design and screening of anti-inflammatory drugs.</div></div>","PeriodicalId":23551,"journal":{"name":"Veterinary microbiology","volume":"307 ","pages":"Article 110628"},"PeriodicalIF":2.4000,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"FCV activates NLRP3 inflammasome through ion-dependent pathway to promote IL-1β secretion\",\"authors\":\"Hongtao Chen , Shihui Zhao , Shanling Liu , Yiming Wei , Yanbing Guo , Kun Gao , Hongze Shao , Han Zhao , Di Bao , Shuang Zhang , Shushuai Yi , Kai Wang , Guixue Hu\",\"doi\":\"10.1016/j.vetmic.2025.110628\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Feline calicivirus (FCV) poses a significant threat to the health of susceptible animals in the global epidemic. The inflammasome plays a crucial role in the inflammatory process induced by pathogens, functioning in resisting their invasion, responding to cellular damage, and maintaining internal environmental homeostasis.FCV infection in cats causes inflammation,and the regulatory mecha-nisms of the NLRP3 inflammasome on inflammatory factors in infected cells urgently require further investigation.This study focuses on this inflammasome as the entry point, focusing on its activation signal that activates IL-1β secretion.Through cellular experiments, it analyzes the molecular mechanisms and logical relationships between this inflammasome, intracellular environ-ment, pyroptosis, the regulation of IL-1β secretion by viral-encoded proteins.The results showed that FCV-infected cells induced the activation and assembly of the NLRP3 inflammasome, thereby activating this signaling. FCV-induced IL-1β secretion was dependent on the activation of this inflammasome. In the early stages of infection, the activation of this inflammasome and IL-1β secretion were dependent on cellular Ca<sup>2 +</sup> influx and K<sup>+</sup> efflux. IL-1β secretion also relied on FCV-induced pyroptosis;The activation of this inflammasome by the FCV-encoded protein p32/LC and the subsequent induction of IL-1β secretion are contingent upon the function of its in mediating cellular Ca<sup>2+</sup> influx and K<sup>+</sup> efflux.In summary, this study demonstrates that following FCV infection of cells, its p32 and LC proteins activate the NLRP3 inflammasome activation signal in a manner dependent on Ca<sup>2+</sup> influx and K<sup>+</sup> efflux,Induce IL-1β secretion. In addition, FCV-induced pyroptosis also triggers the secretion of IL-1β. The findings of this study elucidate the leading to inflammatory mechanisms of FCV from a novel perspective, providing new drug targets for the design and screening of anti-inflammatory drugs.</div></div>\",\"PeriodicalId\":23551,\"journal\":{\"name\":\"Veterinary microbiology\",\"volume\":\"307 \",\"pages\":\"Article 110628\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-06-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Veterinary microbiology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0378113525002639\",\"RegionNum\":2,\"RegionCategory\":\"农林科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Veterinary microbiology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0378113525002639","RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
FCV activates NLRP3 inflammasome through ion-dependent pathway to promote IL-1β secretion
Feline calicivirus (FCV) poses a significant threat to the health of susceptible animals in the global epidemic. The inflammasome plays a crucial role in the inflammatory process induced by pathogens, functioning in resisting their invasion, responding to cellular damage, and maintaining internal environmental homeostasis.FCV infection in cats causes inflammation,and the regulatory mecha-nisms of the NLRP3 inflammasome on inflammatory factors in infected cells urgently require further investigation.This study focuses on this inflammasome as the entry point, focusing on its activation signal that activates IL-1β secretion.Through cellular experiments, it analyzes the molecular mechanisms and logical relationships between this inflammasome, intracellular environ-ment, pyroptosis, the regulation of IL-1β secretion by viral-encoded proteins.The results showed that FCV-infected cells induced the activation and assembly of the NLRP3 inflammasome, thereby activating this signaling. FCV-induced IL-1β secretion was dependent on the activation of this inflammasome. In the early stages of infection, the activation of this inflammasome and IL-1β secretion were dependent on cellular Ca2 + influx and K+ efflux. IL-1β secretion also relied on FCV-induced pyroptosis;The activation of this inflammasome by the FCV-encoded protein p32/LC and the subsequent induction of IL-1β secretion are contingent upon the function of its in mediating cellular Ca2+ influx and K+ efflux.In summary, this study demonstrates that following FCV infection of cells, its p32 and LC proteins activate the NLRP3 inflammasome activation signal in a manner dependent on Ca2+ influx and K+ efflux,Induce IL-1β secretion. In addition, FCV-induced pyroptosis also triggers the secretion of IL-1β. The findings of this study elucidate the leading to inflammatory mechanisms of FCV from a novel perspective, providing new drug targets for the design and screening of anti-inflammatory drugs.
期刊介绍:
Veterinary Microbiology is concerned with microbial (bacterial, fungal, viral) diseases of domesticated vertebrate animals (livestock, companion animals, fur-bearing animals, game, poultry, fish) that supply food, other useful products or companionship. In addition, Microbial diseases of wild animals living in captivity, or as members of the feral fauna will also be considered if the infections are of interest because of their interrelation with humans (zoonoses) and/or domestic animals. Studies of antimicrobial resistance are also included, provided that the results represent a substantial advance in knowledge. Authors are strongly encouraged to read - prior to submission - the Editorials (''Scope or cope'' and ''Scope or cope II'') published previously in the journal. The Editors reserve the right to suggest submission to another journal for those papers which they feel would be more appropriate for consideration by that journal.
Original research papers of high quality and novelty on aspects of control, host response, molecular biology, pathogenesis, prevention, and treatment of microbial diseases of animals are published. Papers dealing primarily with immunology, epidemiology, molecular biology and antiviral or microbial agents will only be considered if they demonstrate a clear impact on a disease. Papers focusing solely on diagnostic techniques (such as another PCR protocol or ELISA) will not be published - focus should be on a microorganism and not on a particular technique. Papers only reporting microbial sequences, transcriptomics data, or proteomics data will not be considered unless the results represent a substantial advance in knowledge.
Drug trial papers will be considered if they have general application or significance. Papers on the identification of microorganisms will also be considered, but detailed taxonomic studies do not fall within the scope of the journal. Case reports will not be published, unless they have general application or contain novel aspects. Papers of geographically limited interest, which repeat what had been established elsewhere will not be considered. The readership of the journal is global.