NLRP3 inflammasome is expressed and functional in mouse brain microglia but not in astrocytes
Open accessAbstract
Neuroinflammation is the local reaction of the brain to infection, trauma, toxic molecules or protein aggregates. The brain resident macrophages, microglia, are able to trigger an appropriate response involving secretion of cytokines and chemokines, resulting in the activation of astrocytes and recruitment of peripheral immune cells. IL-1β plays an important role in this response; yet its production and mode of action in the brain are not fully understood and its precise implication in neurodegenerative diseases needs further characterization. Our results indicate that the capacity to form a functional NLRP3 inflammasome and secretion of IL-1β is limited to the microglial compartment in the mouse brain. We were not able to observe IL-1β secretion from astrocytes, nor do they express all NLRP3 inflammasome components. Microglia were able to produce IL-1β in response to different classical inflammasome activators, such as ATP, Nigericin or Alum. Similarly, microglia secreted IL-18 and IL-1α, two other inflammasome-linked pro-inflammatory factors. Cell stimulation with α-synuclein, a neurodegenerative disease-related peptide, did not result in the release of active IL-1β by microglia, despite a weak pro-inflammatory effect. Amyloid-β peptides were able to activate the NLRP3 inflammasome in microglia and IL-1β secretion occurred in a P2X7 receptor-independent manner. Thus microglia-dependent inflammasome activation can play an important role in the brain and especially in neuroinflammatory conditions.
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Inflammasome signaling in the CNS has been reported in microglia, astrocytes, perivascular brain-resident macrophages, oligodendrocytes, endothelial cells, and neurons.
“Inflammasome signaling in the CNS has also been reported in the microglia, the brain’s critical innate immune cells (206), in astrocytes (207), perivascular brain-resident macrophages (208), oligodendrocytes (209), endothelial cells (210), as well as in neurons (211).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [206]
Stimulation of microglia cell culture with ATP enhances expression of NLRP3, ASC protein and caspase-1 along with enhanced secretion of IL-1β and IL-18 in a NLRP3 inflammasome-dependent manner.
“stimulation of microglia cell culture with ATP enhance the expression of NLRP3, ASC protein and caspase-1 along with enhanced secretion of IL-1β and IL-18 in a NLRP3 inflammasome-dependent manner.”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [153]
The same NLRP3 inflammasome components (ASC, caspase-1 and cytokines) were not observed in astrocytes culture, indicating cell-type specific NLRP3 expression.
“The same NLRP3 inflammasome components (ASC, caspase-1 and cytokines) were not observed in astrocytes culture cell, indicating a cell-type specific NLRP3 expression [153].”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [153]
The effects of ATP in microglia NLRP3 activation were blocked by pre-treatment with KCl, preventing K+ efflux, suggesting requirement of low intracellular K+ for NLRP3 inflammasome activation.
“Additionally, the effects of ATP in microglia NRLP3 activation were blocked by pre-treatment with potassium chloride (KCl), preventing the efflux of K+, suggesting requirement of low concentrations of this ion in the intracellular environment for the activation of NLRP3 inflammasome [153].”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [153]
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- Authors
- Gustin, A., Kirchmeyer, M., Koncina, E., Felten, P., Losciuto, S., Heurtaux, T., Tardivel, A., Heuschling, P., & Dostert, C.
- Affiliations
- University of Luxembourg (LU)
- University of Lausanne (CH)
- Corresponding author
- Dostert, Catherine
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-06-19
- Volume
- 10
- Issue
- 6
- Pages
- e0130624
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4474809
- OpenAlex
- W582182564
- Cited by
- 369
- References
- 55
- Citations by year
- 2026: 21 · 2025: 27 · 2024: 33 · 2023: 38 · 2022: 33 · 2021: 44 · 2020: 59 · 2019: 27 · 2018: 29 · 2017: 37 · 2016: 17 · 2015: 3
- FWCI
- 12.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, cc-by-nc-sa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- SERVAL (Université de Lausanne) (submittedVersion, other-oa)
- Funders
- Université du Luxembourg
- Fonds National de la Recherche Luxembourg
- Université de Lausanne
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- NLRP3 inflammasome, microglia, astrocytes, IL-1β secretion, neuroinflammation, IL-18, IL-1α, alpha-synuclein, amyloid-beta, P2X7 receptor, neurodegenerative diseases
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Astrocytes, Brain, Carrier Proteins, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Mice, Inbred C57BL, Peptide Fragments, Amyloid beta-Peptides, Microglia, Mice, Knockout, Caspase 1, Interleukin-18, Mice, alpha-Synuclein, Interleukin-1alpha, Interleukin-1beta, Receptors, Purinergic P2X7, Inflammasomes
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