ArticlePloS one2015
Prion pathogenesis in the absence of NLRP3/ASC inflammasomes.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Microglia-specific NF-κB signaling is a critical regulator of prion-induced glial inflammation and neuronal loss.PLoS pathogens · 2025Article
- Article
- Genetic analysis of potential biomarkers and therapeutic targets in neuroinflammation from sporadic Creutzfeldt-Jakob disease.Scientific reports · 2023Article
- Gene expression and epigenetic markers of prion diseases.Cell and tissue research · 2023Review
- Adipose-derived mesenchymal stromal cells decrease prion-induced glial inflammation in vitro.Scientific reports · 2022Article
- Review
- Supramolecular organizing centers at the interface of inflammation and neurodegeneration.Frontiers in immunology · 2022Review
- Glial Cells and Brain Diseases: Inflammasomes as Relevant Pathological Entities.Frontiers in cellular neuroscience · 2022Review
- The role of microglia in prion diseases and possible therapeutic targets: a literature review.Prion · 2021Review
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Neurodegenerative Disease and the NLRP3 Inflammasome.Frontiers in pharmacology · 2021Review
- Altered DNA methylation profiles in blood from patients with sporadic Creutzfeldt-Jakob disease.Acta neuropathologica · 2020Article
- The Effects of Immune System Modulation on Prion Disease Susceptibility and Pathogenesis.International journal of molecular sciences · 2020Review
- Epigenetic Mechanisms of Inflammasome Regulation.International journal of molecular sciences · 2020Review
- Focus on the Role of NLRP3 Inflammasome in Diseases.International journal of molecular sciences · 2020Review
- Inflammasomes in neuroinflammatory and neurodegenerative diseases.EMBO molecular medicine · 2019Review
- Type I interferon protects neurons from prions in in vivo models.Brain : a journal of neurology · 2019Article
- NLRs as Helpline in the Brain: Mechanisms and Therapeutic Implications.Molecular neurobiology · 2018Review
- The NLRP3-Caspase 1 Inflammasome Negatively Regulates Autophagy via TLR4-TRIF in Prion Peptide-Infected Microglia.Frontiers in aging neuroscience · 2018Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The accumulation of the scrapie prion protein PrPSc, a misfolded conformer of the cellular prion protein PrPC, is a crucial feature of prion diseases. In the central nervous system, this process is accompanied by conspicuous microglia activation. The NLRP3 inflammasome is a multi-molecular complex which can sense heterogeneous pathogen-associated molecular patterns and culminates in the activation of caspase 1 and release of IL 1β. The NLRP3 inflammasome was reported to be essential for IL 1β release after in vitro exposure to the amyloidogenic peptide PrP106-126 and to recombinant PrP fibrils. We therefore studied the role of the NLRP3 inflammasome in a mouse model of prion infection. Upon intracerebral inoculation with scrapie prions (strain RML), mice lacking NLRP3 (Nlrp3-/-) or the inflammasome adaptor protein ASC (Pycard-/-) succumbed to scrapie with attack rates and incubation times similar to wild-type mice, and developed the classic histologic and biochemical features of prion diseases. Genetic ablation of NLRP3 or ASC did not significantly impact on brain levels of IL 1β at the terminal stage of disease. Our results exclude a significant role for NLRP3 and ASC in prion pathogenesis and invalidate their claimed potential as therapeutic target against prion diseases.
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