Microglia in the degenerating brain are capable of phagocytosis of beads and of apoptotic cells, but do not efficiently remove PrPSc, even upon LPS stimulation
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Despite the phagocytic machinery available to microglia the aberrant amyloid proteins produced during Alzheimer's and prion disease, amyloid‐β and PrP Sc, are inefficiently cleared. We have shown that microglia in the ME7 model of prion disease show morphological evidence of activation, synthesize low levels of pro‐inflammatory cytokines and are primed to produce exaggerated responses to subsequent inflammatory challenges. Whether these microglia engage in significant phagocytic activity in the disease per se, or upon subsequent inflammatory challenge is not clear. In the present study we show transcriptional activation of a large number of scavenger receptors (SRs), matrix metalloproteinases (MMPs), oxidative enzymes, and cathepsins in ME7 animals. Hippocampally‐injected inert latex beads (6 μm) are efficiently phagocytosed by microglia of ME7 prion‐diseased animals, but not by microglia in normal animals. Stimulation of ME7 animals with systemic bacterial endotoxin (lipopolysaccharide, LPS) induced further increases in SR‐A2, MMP3, and urokinase plasminogen activator receptor (uPAR) but decreased, or did not alter, transcription of most phagocytosis‐related genes examined and did not enhance clearance of deposited PrP Sc. Furthermore, intracerebral injection with LPS (0.5 μg) induced marked microglial production of IL‐1β, robust cellular infiltration and marked apoptosis but also did not induce further clearance of PrP Sc. These data indicate that microglia in the prion‐diseased brain are capable of phagocytosis per se, but show limited efficacy in removing PrP Sc even upon marked escalation of CNS inflammation. Furthermore, microglia/macrophages remain IL‐1β‐negative during phagocytosis of apoptotic cells. The data demonstrate that phagocytic activity and pro‐inflammatory microglial phenotype do not necessarily correlate. © 2010 Wiley‐Liss, Inc.
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In our model, the scavenger receptors SCARB1, SCARB2 and AGER were not up-regulated during disease, contrary to previous reports.
“Contrary to previous reports, we did not find the scavenger receptors SCARB1, SCARB2 and AGER to be up-regulated during disease [39].”
From MicroRNA 146a (miR-146a) Is Over-Expressed during Prion Disease and Modulates the Innate Immune Response and the Microglial Activation State (2012) · cites this paper as [39]
The Results section (‘Upregulation of Phagocytosis-Related Genes in ME7 Versus NBH Animals’; page unavailable) reports increased RAGE (AGER) expression during disease, supporting that part of the cited contrast. It reports CD36, SRA2 and CD68 as the other up-regulated scavenger receptors, but does not report up-regulation of SCARB1 or SCARB2. The citing authors’ own failure to find up-regulation is not a finding attributed to this source. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLPS could not further stimulate the PrPSc-degrading function of microglia during disease progression.
“while another stimulator of inflammation, the bacterial lipopolysaccharide (LPS), could not further stimulate their PrPSc-degrading function during disease progression [81].”
From Loss of Homeostatic Microglia Signature in Prion Diseases (2022) · cites this paper as [81]
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- Authors
- Hughes, M. M., Field, R. H., Perry, V. H., Murray, C. L., & Cunningham, C.
- Affiliations
- Trinity College Dublin (IE)
- University of Southampton (GB)
- Corresponding author
- Cunningham, Colm
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2010-09-27
- Volume
- 58
- Issue
- 16
- Pages
- 2017-2030
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC3498730
- OpenAlex
- W1964848350
- Cited by
- 94
- References
- 76
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 10 · 2020: 4 · 2019: 8 · 2018: 6 · 2017: 11 · 2016: 5 · 2015: 4 · 2014: 9 · 2013: 12 · 2012: 11
- FWCI
- 5.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Glia (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (acceptedVersion)
- Funders
- Wellcome Trust (090907)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Prion Diseases and Protein Misfolding
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- microglia, phagocytosis, prion disease, scavenger receptors, lipopolysaccharide, IL-1β, apoptosis, amyloid-beta, matrix metalloproteinases, urokinase-type plasminogen activator receptor, microglial activation, neuroinflammation, latex bead phagocytosis
- MeSH terms
- Animals, Brain, Encephalitis, Female, Gene Expression Regulation, Lipopolysaccharides, Mice, Inbred C57BL, Microspheres, Phagocytosis, Phenotype, Up-Regulation, Prion Diseases, Apoptosis, Microglia, PrPSc Proteins, Mice
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