ArticleMediators of inflammation2014
Porcine reproductive and respiratory syndrome virus induces IL-1β production depending on TLR4/MyD88 pathway and NLRP3 inflammasome in primary porcine alveolar macrophages.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 76 citations in OpenAlex.
- PRRSV infection induces mitochondrial damage and releases mitochondrial dsRNA to activate the NLRP3-dependent inflammatory response.Veterinary research · 2026Article
- Highly pathogenic porcine reproductive and respiratory syndrome virus nonstructural protein 1 interacts with TRAF6 to activate the TAK1/p38/JNK/AP-1 signaling and induce IL-1β.Journal of virology · 2026Article
- Whole-Genome Resequencing-Based Selection-Signal and Association Analyses Prioritize Candidate Genes and Haplotypes for PRRS Resistance-Related Traits in Pigs.Animals : an open access journal from MDPI · 2026Article
- Tylvalosin tartrate inhibits PRRSV replication by suppressing cellular pyroptosis through the TLR4/NF-κB signaling pathway.Journal of virology · 2026Article
- CombinedInternational journal of molecular sciences · 2025Article
- Salvianolic acid A inhibits PRRSV replication via binding to Keap1 to activate the MKRN1-Nrf2-NQO1 pathway.Veterinary research · 2025Article
- Activation and evasion of inflammasomes during viral and microbial infection.Cellular and molecular life sciences : CMLS · 2025Review
- Early boosting of p38 MAPK signaling pathway by lycorine hydrochloride potently inhibits PRRSV proliferation in primary and established cells.Frontiers in microbiology · 2025Article
- Molecular Characterization and Pathogenicity of a Novel Recombinant NADC30-Like PRRSV Strain Isolated From Piglets Inducing Intestinal Inflammation, and Construction of Its Infectious Clone.Transboundary and emerging diseases · 2025Article
- The Genetic Variation of Porcine Reproductive and Respiratory Syndrome Virus Replicase Protein nsp2 Modulates Viral Virulence and Persistence.Journal of virology · 2023Article
- Differential innate immune response of endometrial cells to porcine reproductive and respiratory syndrome virus type 1 versus type 2.PloS one · 2023Article
- Construction of an infectious cloning system of porcine reproductive and respiratory syndrome virus and identification of glycoprotein 5 as a potential determinant of virulence and pathogenicity.Frontiers in microbiology · 2023Article
- Genetic background influences pig responses to porcine reproductive and respiratory syndrome virus.Frontiers in veterinary science · 2023Review
- PRRSV Infection Induces Gasdermin D-Driven Pyroptosis of Porcine Alveolar Macrophages through NLRP3 Inflammasome Activation.Journal of virology · 2022Article
- Peste Des Petits Ruminants Virus N Protein Is a Critical Proinflammation Factor That Promotes MyD88 and NLRP3 Complex Assembly.Journal of virology · 2022Article
- The Antiviral Effect ofInternational journal of molecular sciences · 2022Article
- Neutralization of S100A4 induces stabilization of atherosclerotic plaques: role of smooth muscle cells.Cardiovascular research · 2022Article
- pMGF505-7R determines pathogenicity of African swine fever virus infection by inhibiting IL-1β and type I IFN production.PLoS pathogens · 2021Article
- Damage to intestinal barrier integrity in piglets caused by porcine reproductive and respiratory syndrome virus infection.Veterinary research · 2021Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is an Arterivirus that has been devastating the swine industry worldwide since the late 1980s. Previous studies have reported that PRRSV infection induced the production of IL-1 β . However, the cellular sensors and signaling pathways involved in this process have not been elucidated yet. Here, we studied the mechanisms responsible for the production of IL-1 β in response to highly pathogenic PRRSV. Upon PRRSV infection of primary porcine alveolar macrophages, both mRNA expression and secretion of IL-1 β were significantly increased in a time- and dose-dependent manner. We also investigated the role of several pattern-recognition receptors and adaptor molecules in this response and showed that the TLR4/MyD88 pathway and its downstream signaling molecules, NF- κ B, ERK1/2, and p38 MAPKs, were involved in IL-1 β production during PRRSV infection. Treatment with specific inhibitors or siRNA knockdown assays demonstrated that components of the NLRP3 inflammasome were crucial for IL-1 β secretion but not for IL-1 β mRNA expression. Furthermore, TLR4/MyD88/NF- κ B signaling pathway was involved in PRRSV-induced expression of NLRP3 inflammasome components. Together, our results deciphered the pathways leading from recognition of PRRSV to the production and release of IL-1 β , providing a deeper knowledge of the mechanisms of PRRSV-induced inflammation responses.
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