ArticleJournal of virology2013
Absence of CD14 delays progression of prion diseases accompanied by increased microglial activation.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- Interferon-Stimulated Gene-Mediated Defense Against Prion Infection: Noncanonical Function of Oas1a.Viruses · 2026Review
- Impact of Hematopoietic CD14 on Oxidative Stress during Salt-Sensitive Hypertension and Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Review
- Article
- Review
- Neuroinflammation in Prion Disease.International journal of molecular sciences · 2021Review
- Review
- Microglia in Prion Diseases: Angels or Demons?International journal of molecular sciences · 2020Review
- Administration of FK506 from Late Stage of Disease Prolongs Survival of Human Prion-Inoculated Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- Region-specific glial homeostatic signature in prion diseases is replaced by a uniform neuroinflammation signature, common for brain regions and prion strains with different cell tropism.Neurobiology of disease · 2020Article
- Phenotypic Differences in Primary Murine Microglia Treated with NOD1, NOD2, and NOD1/2 Agonists.Journal of molecular neuroscience : MN · 2020Article
- Core transcriptional regulatory circuits in prion diseases.Molecular brain · 2020Article
- Microbiome Influence in the Pathogenesis of Prion and Alzheimer's Diseases.International journal of molecular sciences · 2019Review
- SARM1 deficiency up-regulates XAF1, promotes neuronal apoptosis, and accelerates prion disease.The Journal of experimental medicine · 2019Article
- Enhancement of binding avidity by bivalent binding enables PrPSc-specific detection by anti-PrP monoclonal antibody 132.PloS one · 2019Article
- Region-Specific Response of Astrocytes to Prion Infection.Frontiers in neuroscience · 2019Article
- Microglia in neurodegeneration.Nature neuroscience · 2018Review
- Inflammatory response of microglia to prions is controlled by sialylation of PrPScientific reports · 2018Article
- Flow Cytometric Detection of PrPJournal of virology · 2018Article
- Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion diseases are fatal neurodegenerative disorders characterized by accumulation of PrP(Sc), vacuolation of neurons and neuropil, astrocytosis, and microglial activation. Upregulation of gene expressions of innate immunity-related factors, including complement factors and CD14, is observed in the brains of mice infected with prions even in the early stage of infections. When CD14 knockout (CD14(-/-)) mice were infected intracerebrally with the Chandler and Obihiro prion strains, the mice survived longer than wild-type (WT) mice, suggesting that CD14 influences the progression of the prion disease. Immunofluorescence staining that can distinguish normal prion protein from the disease-specific form of prion protein (PrP(Sc)) revealed that deposition of PrP(Sc) was delayed in CD14(-/-) mice compared with WT mice by the middle stage of the infection. Immunohistochemical staining with Iba1, a marker for activated microglia, showed an increased microglial activation in prion-infected CD14(-/-) mice compared to WT mice. Interestingly, accompanied by the increased microglial activation, anti-inflammatory cytokines interleukin-10 (IL-10) and transforming growth factor β (TGF-β) appeared to be expressed earlier in prion-infected CD14(-/-) mice. In contrast, IL-1β expression appeared to be reduced in the CD14(-/-) mice in the early stage of infection. Double immunofluorescence staining demonstrated that CD11b- and Iba1-positive microglia mainly produced the anti-inflammatory cytokines, suggesting anti-inflammatory status of microglia in the CD14(-/-) mice in the early stage of infection. These results imply that CD14 plays a role in the disease progression by suppressing anti-inflammatory responses in the brain in the early stage of infection.
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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.