Co-stimulation with IL-1β and TNF-α induces an inflammatory reactive astrocyte phenotype with neurosupportive characteristics in a human pluripotent stem cell model system
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Astrocyte reactivation has been discovered to be an important contributor to several neurological diseases. In vitro models involving human astrocytes have the potential to reveal disease-specific mechanisms of these cells and to advance research on neuropathological conditions. Here, we induced a reactive phenotype in human induced pluripotent stem cell (hiPSC)-derived astrocytes and studied the inflammatory natures and effects of these cells on human neurons. Astrocytes responded to interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) treatment with a typical transition to polygonal morphology and a shift to an inflammatory phenotype characterized by altered gene and protein expression profiles. Astrocyte-secreted factors did not exert neurotoxic effects, whereas they transiently promoted the functional activity of neurons. Importantly, we engineered a novel microfluidic platform designed for investigating interactions between neuronal axons and reactive astrocytes that also enables the implementation of a controlled inflammatory environment. In this platform, selective stimulation of astrocytes resulted in an inflammatory niche that sustained axonal growth, further suggesting that treatment induces a reactive astrocyte phenotype with neurosupportive characteristics. Our findings show that hiPSC-derived astrocytes are suitable for modeling astrogliosis, and the developed in vitro platform provides promising novel tools for studying neuron-astrocyte crosstalk and human brain disease in a dish.
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The neuroprotective phenotype of astrocytes promotes neuronal survival and homeostasis, as these astrocytes secrete neurotrophic factors and anti-inflammatory cytokines.
“Conversely, the “neuroprotective” phenotype of astrocytes promotes neuronal survival and homeostasis, as these astrocytes secrete neurotrophic factors and anti-inflammatory cytokines [184, 187, 188].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [184]
The Introduction (page unavailable) says astrocytes release trophic factors and help maintain homeostasis; the Discussion reports that stimulated astrocytes sustained neuronal viability. But the Discussion describes a broad inflammatory secretion profile and explicitly says the mechanism of neurosupport is unknown. It does not establish that anti-inflammatory cytokines account for the observed support. (LLM, conf=0.88)
Experimental — accuracy not yet measuredMicroglial activation or inflammatory insults induce astrocytes into a reactive state, which can have both neuroprotective and neurotoxic effects.
“Microglial activation or inflammatory insults induce astrocytes into a reactive state, which can have both neuroprotective and neurotoxic effects [17, 183–185].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [184]
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- Authors
- Hyvärinen, T., Hagman, S., Ristola, M., Sukki, L., Veijula, K., Kreutzer, J., Kallio, P., & Narkilahti, S.
- Affiliations
- Tampere University (FI)
- Corresponding author
- Narkilahti, Susanna
- ORCID
- Venue
- Scientific Reports
- Published
- 2019-11-15
- Volume
- 9
- Issue
- 1
- Pages
- 16944-16944
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6858358
- OpenAlex
- W2987198483
- Cited by
- 168
- References
- 66
- Citations by year
- 2026: 18 · 2025: 23 · 2024: 39 · 2023: 16 · 2022: 26 · 2021: 31 · 2020: 14
- FWCI
- 7.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Tampere University Institutional Repository (Tampere University) (submittedVersion, cc-by)
- Funders
- Academy of Finland (312411, 312414, 50191927, 296415)
- Suomen Kulttuurirahasto (00170805, 312414, 50191927, 312411)
- Business Finland (50191927, 312414)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- reactive astrocytes, astrocyte activation, IL-1β, TNF-α, neuroinflammation, microfluidic platform, axon growth
- MeSH terms
- Astrocytes, Cell Communication, Cell Differentiation, Cell Survival, Cells, Cultured, Humans, Neurons, Phenotype, Tumor Necrosis Factor-alpha, Cytokines, Coculture Techniques, Pluripotent Stem Cells, Microfluidic Analytical Techniques, Cell Proliferation, Interleukin-1beta, Induced Pluripotent Stem Cells, Cellular Microenvironment
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