Bifidobacterium breve CBT BR3 is effective at relieving intestinal inflammation by augmenting goblet cell regeneration

J Gastroenterol Hepatol. 2023 Aug;38(8):1346-1354. doi: 10.1111/jgh.16209. Epub 2023 May 8.

Abstract

Background and aim: Bifidobacterium breve was the first bacteria isolated in the feces of healthy infants and is a dominant species in the guts of breast-fed infants. Some strains of B. breve have been shown to be effective at relieving intestinal inflammation, but the modes of action have yet to be elucidated. In this study, we investigated the mechanisms of action of B. breve CBT BR3 isolated from South Korean infant feces in relieving colitis in vitro and in vivo.

Methods: Colitis was induced in mice with dextran sodium sulfate (DSS) and dinitrobenzene sulfonic acid (DNBS). Quantitative reverse-transcription polymerase chain reaction, in vitro FITC-dextran flux permeability assay, and aryl hydrocarbon receptor (AhR) luciferase assay are performed using Caco-2 cells and HT29-Lucia™ AhR cells.

Results: B. breve CBT BR3 was orally administered. B. breve CBT BR3 improved colitis symptoms in both DSS- and DNBS-induced colitis models. B. breve CBT BR3 increased the number of goblet cells per crypt. B. breve increased the mRNA expressions of Notch, Spdef, Muc5, and Il22. The mRNA expressions of Occludin, which encodes a membrane tight-junction protein, and Foxo3, which encodes a protein related to butyrate metabolism, were also increased in the DSS- and DNBS-induced colitis models. B. breve CBT BR3 protected inflammation-induced epithelial cell permeability and improved goblet cell function by inducing aryl hydrocarbon receptor in vitro.

Conclusions: These results indicate that B. breve CBT BR3 is effective at relieving intestinal inflammation by augmenting goblet cell regeneration.

Keywords: Bifidobacterium breve; goblet cell; inflammatory bowel disease; probiotics.

MeSH terms

  • Animals
  • Bifidobacterium breve* / genetics
  • Caco-2 Cells
  • Colitis* / chemically induced
  • Colitis* / metabolism
  • Colitis* / therapy
  • Dextran Sulfate
  • Disease Models, Animal
  • Goblet Cells / metabolism
  • Humans
  • Inflammation / metabolism
  • Inflammation / therapy
  • Intestinal Mucosa
  • Mice
  • Mice, Inbred C57BL
  • RNA, Messenger / genetics
  • Receptors, Aryl Hydrocarbon / metabolism
  • Regeneration

Substances

  • Receptors, Aryl Hydrocarbon
  • 2,4-dinitrofluorobenzene sulfonic acid
  • RNA, Messenger
  • Dextran Sulfate