Microglial Phagocytosis Induced by Fibrillar β-Amyloid and IgGs Are Differentially Regulated by Proinflammatory Cytokines
Open accessAbstract
Microglia undergo a phenotypic activation in response to fibrillar beta-amyloid (fAbeta) deposition in the brains of Alzheimer's disease (AD) patients, resulting in their elaboration of inflammatory molecules. Despite the presence of abundant plaque-associated microglia in the brains of AD patients and in animal models of the disease, microglia fail to efficiently clear fAbeta deposits. However, they can be induced to do so during Abeta vaccination therapy attributable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abeta plaques. We report that proinflammatory cytokines attenuate microglial phagocytosis stimulated by fAbeta or complement receptor 3 and argue that this may, in part, underlie the accumulation of fAbeta-containing plaques within the AD brain. The proinflammatory suppression of fAbeta-elicited phagocytosis is dependent on nuclear factor kappaB activation. Significantly, the proinflammatory cytokines do not inhibit phagocytosis elicited by antibody-mediated activation of FcR, which may contribute to the efficiency of Abeta vaccination-based therapy. Importantly, the proinflammatory suppression of fAbeta phagocytosis can be relieved by the coincubation with anti-inflammatory cytokines, cyclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinflammatory cytokines induce the production of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis. These findings support anti-inflammatory therapies for the treatment of AD.
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Reactive microglia encircle amyloid plaques and sequester Aβ amyloid within their cytoplasm in vitro.
“Initial observations revealed that reactive microglia encircle amyloid plaques and sequester Aβ amyloid within their cytoplasm in vitro [48, 104].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [48]
The Introduction (page unavailable) says activated microglia surround plaques in the Alzheimer’s disease brain. It does not place that observation in vitro; moreover, the Phagocytosis assay section (page unavailable) measures uptake of fluorescent microspheres after Aβ stimulation, not sequestration of Aβ within microglial cytoplasm. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn vivo Aβ removal is critically dependent on microglial activation status.
“However, considerable evidence suggests that in vivo A removal is critically dependent on microglial activation status.33,44 -47”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [33]
The Discussion reports that proinflammatory cytokines inhibit microglial phagocytosis of fibrillar Aβ, supporting a role for microglial state in one clearance pathway. But it says these effects were demonstrated in vitro, cautions that the chronic in vivo situation may differ, and describes other clearance mechanisms operating in parallel. It does not establish that in vivo Aβ removal is critically dependent on microglial activation status. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCX3CR1 modulation of phagocytosis may involve the indirect effect of proinflammatory cytokines which can attenuate phagocytosis.
“Thus, CX3CR1 modulation of phagocytosis may involve the indirect effect of some proinflammatory cytokines which can attenuate phagocytosis (Koenigsknecht-Talboo and Landreth, 2005).”
From CX3CR1 in Microglia Regulates Brain Amyloid Deposition through Selective Protofibrillar Amyloid-β Phagocytosis (2010) · cites this paper as Koenigsknecht-Talboo and Landreth, 2005
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Background
- Authors
- Koenigsknecht-Talboo, J., & Landreth, G. E.
- Affiliations
- Case Western Reserve University (US)
- Case Comprehensive Cancer Center (US)
- ORCID
- Landreth, Gary E.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-09-07
- Volume
- 25
- Issue
- 36
- Pages
- 8240-8249
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6725530
- OpenAlex
- W1974966491
- Cited by
- 477
- References
- 13
- Citations by year
- 2026: 11 · 2025: 22 · 2024: 28 · 2023: 25 · 2022: 36 · 2021: 38 · 2020: 36 · 2019: 25 · 2018: 24 · 2017: 22 · 2016: 23 · 2015: 21 · 2014: 25 · 2013: 23 · 2012: 27
- FWCI
- 6.86
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (AG-20202, R01AG020202)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- microglial phagocytosis, Alzheimer's disease, inflammatory cytokines, IgG receptors, complement receptor 3, NF-κB, prostaglandins, E-prostanoid receptors, ibuprofen, anti-inflammatory therapy, amyloid plaques
- MeSH terms
- Animals, Animals, Newborn, Electric Stimulation, Immunoglobulin G, Inflammation, Interleukin-1, Interleukins, Mice, Inbred C57BL, Peptide Fragments, Phagocytosis, Cytokines, Transforming Growth Factor beta, Amyloid beta-Peptides, Microglia, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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