ArticleFrontiers in immunology2019
NLRP3, NLRP12, and IFI16 Inflammasomes Induction and Caspase-1 Activation Triggered by Virulent HSV-1 Strains Are Associated With Severe Corneal Inflammatory Herpetic Disease.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- PRRSV infection induces mitochondrial damage and releases mitochondrial dsRNA to activate the NLRP3-dependent inflammatory response.Veterinary research · 2026Article
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- From infection to dysfunction: viral triggers and antiviral immune factors in Alzheimer's disease pathology.Frontiers in immunology · 2026Review
- Innate Immunity Never "NODs" Off: NLRs Regulate the Host Anti-Viral Immune Response.Immunological reviews · 2025Review
- Molecular mechanisms of emerging inflammasome complexes and their activation and signaling in inflammation and pyroptosis.Immunological reviews · 2025Review
- Tug of war: innate immunity and herpes simplex keratitis.Frontiers in immunology · 2025Review
- Inflammasomes: potential therapeutic targets in hematopoietic stem cell transplantation.Cell communication and signaling : CCS · 2024Review
- Viral-bacterial co-infections screen in vitro reveals molecular processes affecting pathogen proliferation and host cell viability.Nature communications · 2024Article
- The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis.Clinical microbiology reviews · 2024Review
- Tripartite motif 2b (Journal of virology · 2024Article
- Herpes simplex keratitis: A brief clinical overview.World journal of virology · 2024Review
- Advances in the mechanism of inflammasomes activation in herpes virus infection.Frontiers in immunology · 2024Review
- Overexpression of NLRP12 enhances macrophage immune response and alleviates herpes simplex keratitis.Frontiers in cellular and infection microbiology · 2024Article
- Review
- Sirt1 Negatively Regulates Cellular Antiviral Responses by Preventing the Cytoplasmic Translocation of Interferon-Inducible Protein 16 in Human Cells.Journal of virology · 2023Article
- Cytosolic DNA sensors and glial responses to endogenous DNA.Frontiers in immunology · 2023Review
- SARS-CoV-2 infection increases the gene expression profile for Alzheimer's disease risk.Molecular therapy. Methods & clinical development · 2022Article
- Mechanism of LSD1 in oxygen-glucose deprivation/reoxygenation-induced pyroptosis of retinal ganglion cells via the miR-21-5p/NLRP12 axis.BMC neuroscience · 2022Article
- NLRP3 inflammasome activation mechanism and its role in autoimmune liver disease.Acta biochimica et biophysica Sinica · 2022Review
- Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
The crosstalk between the host's inflammasome system and the invading virulent/less-virulent viruses determines the outcome of the ensuing inflammatory response. An appropriate activation of inflammasomes triggers antiviral inflammatory responses that clear the virus and heal the inflamed tissue. However, an aberrant activation of inflammasomes can result in a harmful and overwhelming inflammation that could damage the infected tissue. The underlying host's immune mechanisms and the viral virulent factors that impact severe clinical inflammatory disease remain to be fully elucidated. In this study, we used herpes simplex virus type 1 (HSV-1), the causative agent of corneal inflammatory herpetic disease, as a model pathogen to determine: (i) Whether and how the virulence of a virus affects the type and the activation level of the inflammasomes; and (ii) How triggering specific inflammasomes translates into protective or damaging inflammatory response. We showed that, in contrast to the less-virulent HSV-1 strains (RE, F, KOS, and KOS63), corneal infection of B6 mice with the virulent HSV-1 strains (McKrae, 17 or KOS79): (i) Induced simultaneous expression of the NLRP3, NLRP12, and IFI16 inflammasomes; (ii) Increased production of the biologically active Caspase-1 and pro-inflammatory cytokines IL-1β and IL-18; (iii) Heightened recruitment into the inflamed cornea of CD45
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Registered trials
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.