AI Article Synopsis

  • Rheumatoid arthritis (RA) is an autoimmune disease influenced by genetic and environmental factors, with recent studies highlighting the gut microbiota's role in its development.
  • Research focused on butyrate, a key metabolite from gut microbiota, reveals it can inhibit histone deacetylases (HDACs), leading to anti-inflammatory effects in an animal model of RA.
  • The study found that butyrate treatment decreased arthritis severity, and its mechanism involved regulating T cell responses and osteoclast activity, particularly through the production of interleukin-10 (IL-10), making butyrate a potential therapeutic option for RA.

Article Abstract

Rheumatoid arthritis (RA) is a systemic autoimmune disease caused by both genetic and environmental factors. Recently, investigators have focused on the gut microbiota, which is thought to be an environmental factor that affects the development of RA. Metabolites secreted by the gut microbiota maintain homeostasis in the gut through various mechanisms [e.g., butyrate, which is one of the major metabolites of gut microbiota, exerts an anti-inflammatory effect by activating G-protein-coupled receptors and inhibiting histone deacetylases (HDACs)]. Here, we focused on the inhibition of the HDACs by butyrate in RA. To this end, we evaluated the therapeutic effects of butyrate in an animal model of autoimmune arthritis. The arthritis score and incidence were lower in the butyrate-treated group compared to the control group. Also, butyrate inhibited HDAC2 in osteoclasts and HDAC8 in T cells, leading to the acetylation of glucocorticoid receptors and estrogen-related receptors α, respectively. Additionally, control of the T17/T cell balance and inhibition of osteoclastogenesis were confirmed by the changes in target gene expression. Interleukin-10 (IL-10) produced by butyrate-induced expanded T cells was critical, as treatment with butyrate did not affect inflammatory arthritis in IL-10-knockout mice. This immune-cell regulation of butyrate was also detected in humans. These findings suggest that butyrate is a candidate agent for the treatment of RA.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6043689PMC
http://dx.doi.org/10.3389/fimmu.2018.01525DOI Listing

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