Role of Butyrate in the expression of Interleukin 4,6,8 in Alzheimer’s disease — The Association Specialists
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Role of Butyrate in the expression of Interleukin 4,6,8 in Alzheimer’s disease (21669)

R.M. Uththara Senarath 1 2 , Lotta Oikari 3 , Prashant Bharadwaj 1 2 , Vijay Jayasena 4 , Juliana Cristina da Silva Chaves 3 , Ralph Martins 1 2 5 6 , Binosha fernando 1 2
  1. School of Medical and Health Sciences, Edith Cowan University, Joondalup, WA, Australia
  2. Australian Alzheimer’s Research Foundation, Ralph and Patricia Sarich Neuroscience Research Institute, Nedlands, WA, Australia
  3. Cellular and Molecular Neurodegeneration, , QIMR Berghofer Medical Research Institute, Brisbaine, QLD, Australia
  4. Nutrition and Food Science, School of Science, Western Sydney University, Penrith , NSW, Australia
  5. Lions Alzheimer’s Foundation, Nedlands, WA, Australia
  6. Department of Biomedical Sciences, Macquarie University, Sydney, NSW, Australia

BackgroundIn Alzheimer's Disease (AD), astrocytes become reactive, which can both protect and harm neurons, contributing to the complex pathology of the disease; research often focuses on how astrocyte dysfunction and neuroinflammation contribute to neuronal damage and cognitive impairment, aiming to find potential therapeutic targets. Butyrate, a short-chain fatty acid produced by gut microbiota, has emerged as a potential therapeutic agent due to its anti-inflammatory properties. This study explores the impact of butyrate on the expression of interleukins IL-4, IL-6, and IL-8 in AD-affected astrocytes and neurons.

MethodologySynthetic Aβ (20μM) and butyrate (100μM) were administered to cultures of astrocytes, neurons and spontaneous cultures derived from iPSCs obtained from a healthy human. Inflammatory marker IL-4,6,8 of these cells was measured using Quantitative PCR and quantified using Legend Plex Human Inflammatory Panel. Statistical analysis was performed using GraphPad Prism version 10.1.2, and one-way ANOVA.

ResultsWhen Aβ-induced cells were treated with butyrate, they exhibited higher expression of IL-8, with a significant increase observed in astrocytes (P<0.05). In contrast, IL-6 expression was low in these cells, with a significant difference noted in neurons and spontaneous cultures. However, IL-4 did not show a significant increase in expression, though there was a tendency for higher expression across all cell types.

ConclusionsThe role of butyrate in modulating the expression of IL-4, IL-6, and IL-8 in AD astrocytes underscores its potential as a therapeutic agent. By selectively influencing cytokine expression, butyrate may contribute to altering the neuroinflammatory milieu in AD. Further research is needed to elucidate this.