Absence of CD14 delays progression of prion diseases accompanied by increased microglial activation
Open accessAbstract
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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Knockout of CD14 leads to prolonged survival with enhanced microglia activation in two different mouse models.
“The knockout of the cluster of differentiation CD14 also led to a prolonged survival with enhanced microglia activation in two different mouse models [77].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [77]
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Innate Immune Status of Glia Modulates Prion Propagation in Early Stage of Infection
Kang, S., Kim, C., Aiken, J. M., & McKenzie, D. I. (2023) · Cells · doi:10.3390/cells12141878 · Cited by 2 · see citing works
Loss of region-specific glial homeostatic signature in prion diseasesPreprint
Makarava, N., Chang, J. C., Molesworth, K., & Baskakov, I. V. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.21203/rs.2.17016/v1 · Cited by 1 · see citing works
Interferon-Stimulated Gene-Mediated Defense Against Prion Infection: Noncanonical Function of Oas1a
Homma, T., & Ishibashi, D. (2026) · Viruses · doi:10.3390/v18090955
- Authors
- Sakai, K., Hasebe, R., Takahashi, Y., Song, C.-H., Suzuki, A., Yamasaki, T., & Horiuchi, M.
- Affiliations
- Hokkaido University (JP)
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2013-12-15
- Volume
- 87
- Issue
- 24
- Pages
- 13433-13445
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- PMC
- PMC3838238
- OpenAlex
- W2077304073
- Cited by
- 37
- References
- 56
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 6 · 2019: 6 · 2018: 3 · 2017: 5 · 2016: 7 · 2015: 1 · 2014: 2
- FWCI
- 1.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Virology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Hokkaido University Collection of Scholarly and Academic Papers (Hokkaido University) (submittedVersion)
- Funders
- Japan Society for the Promotion of Science (23248050)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- prion disease, CD14, microglial activation, prion protein accumulation, disease progression, innate immunity, anti-inflammatory cytokines, IL-10, TGF-beta, IL-1β, neuroinflammation
- MeSH terms
- Animals, Brain, Female, Humans, Mice, Inbred C57BL, Interleukin-10, Prion Diseases, Microglia, Mice, Knockout, Disease Progression, PrPSc Proteins, Lipopolysaccharide Receptors, Mice, Interleukin-1beta
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