Barrier Protection and Recovery Effects of Gut Commensal Bacteria on Differentiated Intestinal Epithelial Cells In Vitro

Nutrients. 2020 Jul 28;12(8):2251. doi: 10.3390/nu12082251.

Abstract

Alterations in the gut microbiota composition play a crucial role in the pathogenesis of inflammatory bowel disease (IBD) as specific commensal bacterial species are underrepresented in the microbiota of IBD patients. In this study, we examined the therapeutic potential of three commensal bacterial species, Faecalibacterium prausnitzii (F. prausnitzii), Roseburia intestinalis (R. intestinalis) and Bacteroides faecis (B. faecis) in an in vitro model of intestinal inflammation, by using differentiated Caco-2 and HT29-MTX cells, stimulated with a pro-inflammatory cocktail consisting of interleukin-1β (IL-1β), tumor necrosis factor-α (TNFα), interferon-γ (IFNγ), and lipopolysaccharide (LPS). Results obtained in this work demonstrated that all three bacterial species are able to recover the impairment of the epithelial barrier function induced by the inflammatory stimulus, as determined by an amelioration of the transepithelial electrical resistance (TEER) and the paracellular permeability of the cell monolayer. Moreover, inflammatory stimulus increased claudin-2 expression and decreased occludin expression were improved in the cells treated with commensal bacteria. Furthermore, the commensals were able to counteract the increased release of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) induced by the inflammatory stimulus. These findings indicated that F. prausnitzii, R. intestinalis and B. faecis improve the epithelial barrier integrity and limit inflammatory responses.

Keywords: Bacteroides faecis; Caco-2 cells; Faecalibacterium prausnitzii; HT29-MTX cells; IBD; Roseburia intestinalis; commensal bacteria; tight junction proteins; transepithelial electrical resistance (TEER).

MeSH terms

  • Bacteroides*
  • Caco-2 Cells
  • Chemokine CCL2 / metabolism
  • Claudin-2
  • Clostridiales*
  • Electric Impedance
  • Epithelial Cells / microbiology*
  • Faecalibacterium prausnitzii*
  • Gastrointestinal Microbiome / physiology*
  • HT29 Cells
  • Humans
  • Inflammatory Bowel Diseases / microbiology*
  • Interferon-gamma / administration & dosage
  • Interleukin-1beta / administration & dosage
  • Interleukin-8 / metabolism
  • Intestinal Mucosa / microbiology
  • Lipopolysaccharides / administration & dosage
  • Occludin / metabolism
  • Permeability
  • Tumor Necrosis Factor-alpha / administration & dosage

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • Claudin-2
  • Interleukin-1beta
  • Interleukin-8
  • Lipopolysaccharides
  • Occludin
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma

Supplementary concepts

  • Bacteroides faecis
  • Roseburia intestinalis

Grants and funding