Toll‐like receptor 4 is required for α‐synuclein dependent activation of microglia and astroglia
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Alpha‐synucleinopathies (ASP) are neurodegenerative disorders, characterized by accumulation of misfolded α‐synuclein, selective neuronal loss, and extensive gliosis. It is accepted that microgliosis and astrogliosis contribute to the disease progression in ASP. Toll‐like receptors (TLRs) are expressed on cells of the innate immune system, including glia, and TLR4 dysregulation may play a role in ASP pathogenesis. In this study we aimed to define the involvement of TLR4 in microglial and astroglial activation induced by different forms of α‐synuclein (full length soluble, fibrillized, and C‐terminally truncated). Purified primary wild type (TLR4+/+) and TLR4 deficient (TLR4−/−) murine microglial and astroglial cell cultures were treated with recombinant α‐synuclein and phagocytic activity, NFκB nuclear translocation, cytokine release, and reactive oxygen species (ROS) production were measured. We show that TLR4 mediates α‐synuclein‐induced microglial phagocytic activity, pro‐inflammatory cytokine release, and ROS production. TLR4−/− astroglia present a suppressed pro‐inflammatory response and decreased ROS production triggered by α‐synuclein treatment. However, the uptake of α‐synuclein by primary astroglia is not dependent on TLR4 expression. Our results indicate the C‐terminally truncated form as the most potent inductor of TLR4‐dependent glial activation. The current findings suggest that TLR4 plays a modulatory role on glial pro‐inflammatory responses and ROS production triggered by α‐synuclein. In contrast to microglia, the uptake of alpha‐synuclein by astroglia is not dependent on TLR4. Our data provide novel insights into the mechanisms of α‐synuclein‐induced microglial and astroglial activation which may have an impact on understanding the pathogenesis of ASP. © 2012 Wiley Periodicals, Inc.
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α-synuclein can trigger TLR4 or TLR2 activation in cultured glia, leading to an increase in inflammatory gene transcription.
“Previous reports showed α-synuclein can trigger TLR4 or TLR2 activation in cultured glia, which leads to an increase in inflammatory gene transcription19,40,41.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [40]
The Results (page unavailable) show that α-synuclein treatment caused TLR4-dependent NF-κB nuclear translocation and increased inflammatory cytokine release in cultured murine glia. The paper measured cytokine release, not an increase in inflammatory gene transcription; its experiments address TLR4 rather than TLR2. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTLR4 is required for NF-κB activation in response to various forms of α-synuclein.
“TLR4 was required for NF-κB activation, and increased inflammation and phagocytic activity in response to various forms of α-synuclein40,41,56.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [40]
TLR4 is required for increased inflammation in response to various forms of α-synuclein.
“TLR4 was required for NF-κB activation, and increased inflammation and phagocytic activity in response to various forms of α-synuclein40,41,56.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [40]
TLR4 is required for increased phagocytic activity in response to various forms of α-synuclein.
“TLR4 was required for NF-κB activation, and increased inflammation and phagocytic activity in response to various forms of α-synuclein40,41,56.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [40]
α-synuclein aggregates induce microglial activation in a TLR-4 dependent manner.
“For instance, α -synuclein aggregates induce microglial activation (Boza-Serrano et al., 2014) in a TLR-4 dependent manner (Fellner et al., 2013).”
From TET2 Regulates the Neuroinflammatory Response in Microglia (2019) · cites this paper as Fellner et al., 2013
Oligomeric α-syn directly engages TLR1/2 and TLR4 to induce a pro-inflammatory M1 phenotype.
“Oligomeric α-syn directly engages TLR1/2 and TLR4 to induce a pro-inflammatory M1 phenotype.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [246]
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- Authors
- Fellner, L., Irschick, R., Schanda, K., Reindl, M., Klimaschewski, L., Poewe, W., Wenning, G. K., & Stefanova, N.
- Affiliations
- Innsbruck Medical University (AT)
- Corresponding author
- Stefanova, Nadia
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2012-10-25
- Volume
- 61
- Issue
- 3
- Pages
- 349-360
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC3568908
- OpenAlex
- W2019863741
- Cited by
- 697
- References
- 64
- Citations by year
- 2026: 31 · 2025: 45 · 2024: 80 · 2023: 54 · 2022: 59 · 2021: 89 · 2020: 79 · 2019: 54 · 2018: 53 · 2017: 42 · 2016: 31 · 2015: 34 · 2014: 31 · 2013: 14
- FWCI
- 12.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Glia (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Austrian Science Fund (F4404, P19989)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- TLR4, alpha-synuclein, synucleinopathies, microglial activation, astroglial activation, microglial phagocytosis, reactive oxygen species, inflammatory cytokines, NF-κB nuclear translocation, glial activation, neuroinflammation
- MeSH terms
- Animals, Astrocytes, Cells, Cultured, Gliosis, Inflammation, Phagocytosis, Tumor Necrosis Factor-alpha, Interleukin-6, NF-kappa B, Reactive Oxygen Species, Microglia, Mice, Knockout, Protein Transport, Toll-Like Receptor 4, Mice, alpha-Synuclein, Chemokine CXCL1
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