Publication

Differential Phagocytic Properties of CD45(low) Microglia and CD45(high) Brain Mononuclear Phagocytes-Activation and Age-Related Effects

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Last modified
  • 03/14/2025
Type of Material
Authors
    Srikant Rangaraju, Emory UniversitySyed A. Raza, Emory UniversityNoel Xiang'An Li, Emory UniversityRanjita Betarbet, Emory UniversityEric B Dammer, Emory UniversityDuc Duong, Emory UniversityJames J Lah, Emory UniversityNicholas Seyfried, Emory UniversityAllan I Levey, Emory University
Language
  • English
Date
  • 2018-03-02
Publisher
  • Frontiers Media
Publication Version
Copyright Statement
  • © 2018 Rangaraju, Raza, Li, Betarbet, Dammer, Duong, Lah, Seyfried and Levey.
License
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 1664-3224
Volume
  • 9
Issue
  • MAR
Start Page
  • 405
End Page
  • 405
Grant/Funding Information
  • This work was supported by: Emory Alzheimer’s Disease Research Center Grant (P50 AG025688), American Brain Foundation Award (#00042351), NINDS K08 (NS099474-1), Emory Neuroscience NINDS Core facilities grant (P30 NS055077), 1U01AG046161, NSF CHE-1507932, and NSF/DMR-BSF 1610377.
  • The work was also supported by the Emory flow cytometry core facility.
Supplemental Material (URL)
Abstract
  • In the central nervous system (CNS), microglia are innate immune mononuclear phagocytes (CNS MPs) that can phagocytose infectious particles, apoptotic cells, neurons, and pathological protein aggregates, such as Aβ in Alzheimer's disease (AD). While CD11b + CD45 low microglia account for the majority of CNS MPs, a small population of CD11b + CD45 high CNS MPs is also recognized in AD that surround Aβ plaques. These transcriptionally and pathologically unique CD45 high cells have unclear origin and undefined phagocytic characteristics. We have comprehensively validated rapid flow cytometric assays of bulk-phase and amyloid β fibril (fAβ) phagocytosis and applied these to study acutely isolated CNS MPs. Using these methods, we provide novel insights into differential abilities of CD11b + CD45 low and CD45 high CNS MPs to phagocytose macroparticles and fAβ under normal, acute, and chronic neuroinflammatory states. CD45 high CNS MPs also highly upregulate TREM2, CD11c, and several disease-associated microglia signature genes and have a higher phagocytic capacity for Aβ as compared to CD45 low microglia in the 5xFAD mouse model of AD that becomes more apparent with aging. Our data suggest an overall pro-phagocytic and protective role for CD11b + CD45 high CNS MPs in neurodegeneration, which if promoted, could be beneficial.
Author Notes
Keywords
Research Categories
  • Biology, Neuroscience
  • Chemistry, Biochemistry
  • Chemistry, General

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