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Interleukin-10 deficiency exacerbates inflammation-induced tau pathology
Lea L Weston1, Shanya Jiang1, Devon Chisholm1
1Department of Molecular Genetics and Microbiology, University of New Mexico, MSC08 4660, 1 University of New Mexico, Albuquerque, NM, 87131, USA.
Journal of Neuroinflammation
|July 19, 2021
Summary
Removing interleukin-10 (IL-10) exacerbates neuroinflammation and tau pathology during acute inflammation. Loss of IL-10 leads to increased tau hyperphosphorylation and neurodegeneration, highlighting IL-10's protective role.
Area of Science:
- Neuroscience
- Immunology
Background:
- Hyperphosphorylated tau is linked to cognitive decline and neuroinflammation in Alzheimer's disease and tauopathies.
- The specific role of inflammation and anti-inflammatory treatments in tauopathies remains unclear.
Purpose of the Study:
- To investigate the effect of removing anti-inflammatory interleukin-10 (IL-10) on neuronal tau pathology during an acute inflammatory challenge.
Main Methods:
- Systemic inflammation was induced in IL-10-deficient (Il10-/-) and control (Il10+/+) mice using lipopolysaccharide (LPS).
- Microglial activation, tau phosphorylation, and cytokine expression were analyzed.
- Tau phosphorylation was quantified using Western blotting and immunohistochemistry.
Main Results:
- Genetic deletion of IL-10 significantly increased LPS-induced tau hyperphosphorylation compared to controls.
- LPS-treated Il10-/- mice exhibited signs of neurodegeneration.
- IL-6 was upregulated in Il10-/- mice, and direct IL-6 treatment induced tau hyperphosphorylation in primary neurons.
Conclusions:
- Loss of IL-10 activates microglia and enhances IL-6 production.
- This leads to increased tau hyperphosphorylation on Alzheimer's disease-relevant epitopes following acute systemic inflammation.
