Unique inflammatory RNA profiles of microglia in Creutzfeldt–Jakob disease
- 13 January 2003
- journal article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences of the United States of America
- Vol. 100 (2), 675-679
- https://doi.org/10.1073/pnas.0237313100
Abstract
Previous studies in Creutzfeldt-Jakob disease (CJD) have shown that myeloid cells in the periphery as well as derivative microglial cells in the brain are infectious. Microglia can show an activated phenotype before prion protein (PrP) pathology is detectable in brain, and isolated infectious microglia contain very little PrP. To find whether a set of inflammatory genes are significantly induced or suppressed with infection, we analyzed RNA from isolated microglia with relevant cDNA arrays, and identified approximately 30 transcripts not previously examined in any transmissible spongiform encephalopathy. This CJD expression profile contrasted with that of uninfected microglia exposed to prototypic inflammatory stimuli such as lipopolysaccharide and IFN-gamma, as well as PrP amyloid. These findings underscore inflammatory pathways evoked by the infectious agent in brain. Transcript profiles unique for CJD microglia and other myeloid cells provide opportunities for more sensitive preclinical diagnoses of infectious and noninfectious neurodegenerative diseases.Keywords
This publication has 36 references indexed in Scilit:
- Recognition of the Measles Virus Nucleocapsid as a Mechanism of IRF-3 ActivationJournal of Virology, 2002
- The interferon-α/β system in antiviral responses: a multimodal machinery of gene regulation by the IRF family of transcription factorsCurrent Opinion in Immunology, 2002
- Apolipoprotein C-I Expression in the Brain in Alzheimer's DiseaseNeurobiology of Disease, 2001
- The CD100–CD72 interaction: a novel mechanism of immune regulationTrends in Immunology, 2001
- Identification of Genes Involved in the Host Response to Neurovirulent Alphavirus InfectionJournal of Virology, 2001
- Cell surface receptors Ly-9 and CD84 recruit the X-linked lymphoproliferative disease gene product SAPBlood, 2001
- Role of microglia and host prion protein in neurotoxicity of a prion protein fragmentNature, 1996
- Cholesterol depletion and modification of COOH-terminal targeting sequence of the prion protein inhibit formation of the scrapie isoform [published erratum appears in J Cell Biol 1995 Jul;130(2):501]The Journal of cell biology, 1995
- Scrapie-associated fibrils in Creutzfeldt–Jakob diseaseNature, 1983
- Failure to Modify Scrapie in Mice by Administration of Interferon or Anti-interferon GlobulinJournal of General Virology, 1983