Lactobacillus casei prevents impaired barrier function in intestinal epithelial cells

APMIS. 2011 Jan;119(1):49-56. doi: 10.1111/j.1600-0463.2010.02691.x. Epub 2010 Oct 25.

Abstract

The exact effect of probiotics on epithelial barrier function is not well understood. The aims of this study were to evaluate cytokine-induced epithelial barrier dysfunction in intestinal epithelial cells (IECs) and to study the role of probiotics in the prevention of epithelial barrier dysfunction. Caco-2 cells grown on transwell chambers were stimulated with tumor necrosis factor (TNF)-α or interferon (IFN)-γ basolaterally. Probiotic, Lactobacillus casei, was added 1 h before cytokine stimulation. MAPK inhibitors were added 15 min before L. casei stimulation. The electrical resistance and paracellular permeability of Caco-2 monolayers were measured. Distribution of zonula occludens (ZO)-1 protein was assessed by immunofluorescence, and Western blot analyses for ZO-1, p-Akt, and toll-like receptor (TLR) 2 were performed. Both TNF-α and IFN-γ stimulation on Caco-2 cells decreased transepithelial resistance (TER), increased epithelial permeability, and decreased ZO-1 expression of Caco-2 cells. In contrast, pretreatment of L. casei reversed the cytokine-induced dysfunction of TER, epithelial permeability, and ZO-1 expression. Reversal of cytokine-induced dysfunction of TER and intestinal permeability by L. casei was abrogated with MAPK inhibitor treatment. Lactobacillus casei stimulation on Caco-2 cells increased TLR2 and p-Akt expression. Probiotic, L. casei, prevents cytokine-induced epithelial barrier dysfunctions in IECs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Butadienes / pharmacology
  • Caco-2 Cells
  • Chromones / pharmacology
  • Humans
  • Imidazoles / pharmacology
  • Interferon-gamma / pharmacology
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / enzymology
  • Intestinal Mucosa / metabolism*
  • Intestinal Mucosa / microbiology
  • Lacticaseibacillus casei*
  • Membrane Proteins / metabolism
  • Microscopy, Confocal
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / metabolism*
  • Morpholines / pharmacology
  • Nitriles / pharmacology
  • Phosphoproteins / metabolism
  • Probiotics / pharmacology*
  • Protein Kinase Inhibitors / pharmacology
  • Proto-Oncogene Proteins c-akt / metabolism
  • Pyridines / pharmacology
  • Toll-Like Receptor 2 / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology
  • Zonula Occludens-1 Protein

Substances

  • Butadienes
  • Chromones
  • Imidazoles
  • Membrane Proteins
  • Morpholines
  • Nitriles
  • Phosphoproteins
  • Protein Kinase Inhibitors
  • Pyridines
  • TJP1 protein, human
  • TLR2 protein, human
  • Toll-Like Receptor 2
  • Tumor Necrosis Factor-alpha
  • U 0126
  • Zonula Occludens-1 Protein
  • 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
  • Interferon-gamma
  • Proto-Oncogene Proteins c-akt
  • Mitogen-Activated Protein Kinases
  • SB 203580