Oat-Derived β-Glucans Induced Trained Immunity Through Metabolic Reprogramming

Inflammation. 2020 Aug;43(4):1323-1336. doi: 10.1007/s10753-020-01211-2.

Abstract

Trained immunity has been recently identified in innate immune cells, which undergo long-term epigenetic and metabolic reprogramming after exposure to pathogens for protection from secondary infections. (1, 3)/(1, 6)-β-glucan derived from fungi can induce potent trained immunity; however, the effect of (1, 3)/(1, 4)-β-glucan (rich in dietary fiber oat) on trained immunity has not been reported. In the present study, two cell culture systems for trained immunity induction were validated in monocytes/macrophages from mouse bone myeloid and human THP-1 cells exposed to positive inducers of trained immunity, including β-glucan from Trametes versicolor or human-oxidized low-density lipoprotein. Primed with oat β-glucan, the mRNA expression and production of TNF-α and IL-6 significantly increased in response to re-stimulation of TLR-4/2 ligands. Moreover, the expression of several key enzymes in glycolytic pathway and tricarboxylic acid cycle was significantly upregulated. In addition, inhibiting these enzymes decreased the production of TNF-α and IL-6 boosted by oat β-glucan. These results show that oat β-glucan induces trained immunity through metabolic reprogramming. This provides important evidence that dietary fiber can maintain the long-term responsiveness of the innate immune system, which may benefit for prevention of infectious diseases or cancers.

Keywords: Dietary fiber; Innate immune memory; Macrophages; Monocytes; Trained immunity; β-Glucan.

MeSH terms

  • Animals
  • Cellular Reprogramming / drug effects
  • Cellular Reprogramming / physiology*
  • Humans
  • Immunity, Innate / drug effects
  • Immunity, Innate / physiology*
  • Inflammation Mediators / immunology
  • Inflammation Mediators / metabolism
  • Macrophages / drug effects
  • Macrophages / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Monocytes / drug effects
  • Monocytes / physiology*
  • beta-Glucans / pharmacology*

Substances

  • Inflammation Mediators
  • beta-Glucans
  • beta-glucan, (1-3)(1-4)-