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Butyrate and trichostatin A attenuate nuclear factor kappaB activation and tumor necrosis factor alpha secretion and

Makoto Usami1, Kazunori Kishimoto, Atsushi Ohata

  • 1Division of Surgical Metabolism, Faculty of Health Science, Kobe University School of Medicine, Kobe, Japan. musa@ams.kobe-u.ac.jp

Nutrition Research (New York, N.Y.)
|December 17, 2008
PubMed

Insights

Short-chain fatty acids like butyrate and propionate, and trichostatin A, reduce tumor necrosis factor-alpha (TNF-alpha) secretion and nuclear factor kappaB (NF-kappaB) activation by influencing prostaglandin E2 (PGE2) pathways.

Area of Science:

  • Immunology
  • Molecular Biology
  • Biochemistry

Background:

  • Pro-inflammatory responses are critical in many diseases.
  • Short-chain fatty acids (SCFAs) and histone deacetylase inhibitors (HDACi) modulate immune cell function.
  • Tumor necrosis factor-alpha (TNF-alpha) and prostaglandin E2 (PGE2) are key inflammatory mediators.

Purpose of the Study:

  • To investigate the effects of SCFAs (butyrate, propionate, acetate) and TSA on TNF-alpha and PGE2 secretion and NF-kappaB activation in lipopolysaccharide-stimulated peripheral blood mononuclear cells.
  • To elucidate the mechanisms underlying SCFA-mediated regulation of inflammatory responses.

Main Methods:

  • Peripheral blood mononuclear cells were treated with SCFAs, tributyrin, or TSA.
  • TNF-alpha, PGE2, and NF-kappaB activation were measured.
  • Inhibitors of cyclooxygenase (COX) and lipoxygenase (LOX) pathways were used to explore mechanisms.

Main Results:

  • Butyrate, propionate, acetate, and TSA down-regulated TNF-alpha secretion.
  • All tested compounds up-regulated PGE2 secretion.
  • Butyrate, propionate, and TSA inhibited NF-kappaB activation.
  • Specific COX and LOX inhibitors differentially affected SCFA actions on TNF-alpha secretion.

Conclusions:

  • Butyrate, propionate, and TSA inhibit TNF-alpha production and NF-kappaB activation, partly via PGE2 modulation.
  • Butyrate and propionate mechanisms involve histone deacetylation.
  • Acetate's anti-inflammatory effect may involve lipoxygenase activation.
  • SCFAs offer potential therapeutic strategies for inflammatory conditions.

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