ArticleFrontiers in cellular and infection microbiology2018
Activation of Interleukin-1β Release by the Classical Swine Fever Virus Is Dependent on the NLRP3 Inflammasome, Which Affects Virus Growth in Monocytes.
Article in Frontiers in cellular and infection microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- The Battle Between Japanese Encephalitis Virus and Host Innate Immune System: Evasion and Response.Viruses · 2026Review
- Activation of IL-1 and IL-18 induced by Mycobacterium neoaurum and bacillus calmette-guérin are dependent on the NLRP3 and AIM2 inflammasome.Veterinary research communications · 2026Article
- Strategies of Classical Swine Fever Immune Evasion.International journal of molecular sciences · 2025Review
- The Interplay Between Viral Infection and Cell Death: A Ping-Pong Effect.Advances in virology · 2025Review
- Advances in research on the impact and mechanisms of pathogenic microorganism infections on pyroptosis.Frontiers in microbiology · 2024Review
- High-level production of nervonic acid in the oleaginous yeast Yarrowia lipolytica by systematic metabolic engineering.Communications biology · 2023Article
- High-resolution kinetic characterization of the RIG-I-signaling pathway and the antiviral response.Life science alliance · 2023Article
- Article
- Inflammasome activation by viral infection: mechanisms of activation and regulation.Frontiers in microbiology · 2023Review
- Transcriptome analysis of PK-15 cells expressing CSFV NS4A.BMC veterinary research · 2022Article
- Article
- Molecular Mechanism and Role of Japanese Encephalitis Virus Infection in Central Nervous System-Mediated Diseases.Viruses · 2022Review
- Promiscuous Inflammasomes: The False Dichotomy of RNA/DNA Virus-Induced Inflammasome Activation and Pyroptosis.Viruses · 2022Review
- Activation of the NLRP3 inflammasome and elevation of interleukin-1β secretion in infection by sever fever with thrombocytopenia syndrome virus.Scientific reports · 2022Article
- Porcine Gasdermin D Is a Substrate of Caspase-1 and an Executioner of Pyroptosis.Frontiers in immunology · 2022Article
- A bi-directional dialog between vascular cells and monocytes/macrophages regulates tumor progression.Cancer metastasis reviews · 2021Review
- Article
- Expression of recombinant classical swine fever virus E2 glycoprotein by endogenous Txnip promoter in stable transgenic CHO cells.Engineering in life sciences · 2020Article
- Newcastle disease virus RNA-induced IL-1β expression via the NLRP3/caspase-1 inflammasome.Veterinary research · 2020Article
- The Role of Autophagy and Autophagy Receptor NDP52 in Microbial Infections.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Classical swine fever virus (CSFV) is a classic Flavivirus that causes the acute, febrile, and highly contagious disease known as classical swine fever (CSF). Inflammasomes are molecular platforms that trigger the maturation of proinflammatory cytokines to engage innate immune defenses that are induced upon cellular infection or stress. However, the relationship between the inflammasome and CSFV infection has not been thoroughly characterized. To understand the function of the inflammasome response to CSFV infection, we infected porcine peripheral blood monocytes (PBMCs) with CSFV. Our results indicated that CSFV infection induced both the generation of pro-interleukin-1β (pro-IL-1β) and its processing in monocytes, leading to the maturation and secretion of IL-1β through the activation of caspase 1. Moreover, CSFV infection in PBMCs induced the production and cleavage of gasdermin D (GSDMD), which is an inducer of pyroptosis. Additional studies showed that CSFV-induced IL-1β secretion was mediated by NLRP3 and that CSFV infection could sufficiently activate the assembly of the NLRP3 inflammasome in monocytes. These results revealed that CSFV infection inhibited the expression of NLRP3, and knockdown of NLRP3 enhanced the replication of CSFV. In conclusion, these findings demonstrate that the NLRP3 inflammasome plays an important role in the innate immune response to CSFV infection.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.