Insensitivity of astrocytes to interleukin 10 signaling following peripheral immune challenge results in prolonged microglial activation in the aged brain
Open accessAbstract
Immune-activated microglia from aged mice produce exaggerated levels of cytokines. Despite high levels of microglial interleukin (IL)-10 in the aged brain, neuroinflammation was prolonged and associated with depressive-like deficits. Because astrocytes respond to IL-10 and, in turn, attenuate microglial activation, we investigated if astrocyte-mediated resolution of microglial activation was impaired with age. Here, aged astrocytes had a dysfunctional profile with higher glial fibrillary acidic protein, lower glutamate transporter expression, and significant cytoskeletal re-arrangement. Moreover, aged astrocytes had reduced expression of growth factors and IL-10 receptor-1 (IL-10R1). After in vivo lipopolysaccharide immune challenge, aged astrocytes had a molecular signature associated with reduced responsiveness to IL-10. This IL-10 insensitivity of aged astrocytes resulted in a failure to induce IL-10R1 and transforming growth factor β and resolve microglial activation. In addition, adult astrocytes reduced microglial activation when co-cultured ex vivo, whereas aged astrocytes did not. Consistent with the aging studies, IL-10R(KO) astrocytes did not augment transforming growth factor β after immune challenge and failed to resolve microglial activation. Collectively, a major cytokine-regulatory loop between activated microglia and astrocytes is impaired in the aged brain.
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Aging was associated with reduced IL-10 receptor on aged astrocytes that resulted in a failure to resolve microglia activation in the aged brain.
“Aging was associated with reduced IL-10 receptor on aged astrocytes that resulted in a failure to resolve microglia activation in the aged brain (Norden et al, 2016).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Norden et al, 2016
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- Authors
- Norden, D. M., Trojanowski, P. J., Walker, F. R., & Godbout, J. P.
- Affiliations
- The Ohio State University (US)
- University of Newcastle Australia (AU)
- Corresponding author
- Godbout, Jonathan P.
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 44
- Pages
- 22-41
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC5467746
- OpenAlex
- W2343167511
- Cited by
- 73
- References
- 86
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 9 · 2023: 5 · 2022: 10 · 2021: 9 · 2020: 9 · 2019: 5 · 2018: 6 · 2017: 5 · 2016: 2
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- NOVA (University of Newcastle Australia) (submittedVersion)
- Funders
- NIA (R01-AG-033028)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- astrocytes, IL-10, microglial activation, neuroinflammation, brain aging, IL-10 receptor 1, TGF-beta, lipopolysaccharide challenge, glial fibrillary acidic protein, glutamate transporters, astrocyte-microglia interaction, depression-like behavior, cytokine signaling
- MeSH terms
- Aging, Animals, Astrocytes, Brain, Cells, Cultured, Glial Fibrillary Acidic Protein, Lipopolysaccharides, Mice, Inbred BALB C, Mice, Inbred C57BL, Signal Transduction, Transforming Growth Factor beta, Interleukin-10, Microglia, Coculture Techniques, Amino Acid Transport System X-AG, Interleukin-10 Receptor alpha Subunit
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