Interleukin-10 deficiency exacerbates inflammation-induced tau pathology
Open accessAbstract
Background: The presence of hyperphosphorylated microtubule-associated protein tau is strongly correlated with cognitive decline and neuroinflammation in Alzheimer’s disease and related tauopathies. However, the role of inflammation and anti-inflammatory interventions in tauopathies is unclear. Our goal was to determine if removing anti-inflammatory interleukin-10 (IL-10) during an acute inflammatory challenge has any effect on neuronal tau pathology. Methods: We induce systemic inflammation in Il10- deficient ( Il10 − / − ) versus Il10 + /+ (Non-Tg) control mice using a single intraperitoneal (i.p.) injection of lipopolysaccharide (LPS) to examine microglial activation and abnormal hyperphosphorylation of endogenous mouse tau protein. Tau phosphorylation was quantified by Western blotting and immunohistochemistry. Microglial morphology was quantified by skeleton analysis. Cytokine expression was determined by multiplex electro chemiluminescent immunoassay (MECI) from Meso Scale Discovery (MSD). Results: Our findings show that genetic deletion of Il10 promotes enhanced neuroinflammation and tau phosphorylation. First, LPS-induced tau hyperphosphorylation was significantly increased in Il10 − / − mice compared to controls. Second, LPS-treated Il10 − / − mice showed signs of neurodegeneration. Third, LPS-treated Il10 − / − mice showed robust IL-6 upregulation and direct treatment of primary neurons with IL-6 resulted in tau hyperphosphorylation on Ser396/Ser404 site. Conclusions: These data support that loss of IL-10 activates microglia, enhances IL-6, and leads to hyperphosphorylation of tau on AD-relevant epitopes in response to acute systemic inflammation.
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IL-10 deficiency has been shown to exacerbate Tau pathology.
“IL-10 deficiency has also been shown to exacerbate Tau pathology [41].”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [41]
IL-10 deletion activates microglia, increases IL-6 production, and leads to tau hyperphosphorylation in response to acute systemic inflammation.
“Another study demonstrates that IL-10 deletion activates microglia, increases IL-6 production, and leads to tau hyperphosphorylation in response to acute systemic inflammation [165].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [165]
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Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation
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“Interestingly, IL-10 deficiency has also been shown to exacerbate Tau pathology [41].”
Background
- Authors
- Weston, L. L., Jiang, S., Chisholm, D., Jantzie, L. L., & Bhaskar, K.
- Affiliations
- University of New Mexico (US)
- Johns Hopkins University (US)
- Corresponding author
- Bhaskar, Kiran
- Venue
- Journal of Neuroinflammation
- Published
- 2021-07-18
- Volume
- 18
- Issue
- 1
- Pages
- 161-161
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC8286621
- OpenAlex
- W3184667630
- Cited by
- 69
- References
- 77
- Citations by year
- 2026: 12 · 2025: 20 · 2024: 11 · 2023: 15 · 2022: 11
- FWCI
- 5.81
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Allergy and Infectious Diseases (T32AI007538)
- National Institute of Neurological Disorders and Stroke (R01NS083704, RF1NS083704)
- National Institute of General Medical Sciences (P20GM121176)
- National Institute on Aging (P20AG068077)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- IL-10, tau hyperphosphorylation, neuroinflammation, tauopathy, Alzheimer's disease, microglial activation, lipopolysaccharide-induced inflammation, interleukin-6, anti-inflammatory cytokines, neurodegeneration
- MeSH terms
- Animals, Disease Models, Animal, Immunohistochemistry, Inflammation, Lipopolysaccharides, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Phosphorylation, Interleukin-6, Cytokines, Interleukin-10, tau Proteins, Microglia, Cell Culture Techniques, Tauopathies, 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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