title: Lactobacillus casei prevents impaired barrier function in intestinal epithelial cells.
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.
authors.affiliation: Department of Internal Medicine, Hanyang University Guri Hospital, Gyeonggi-Do, Korea.
authors.forename: Chang Soo
authors.initials: CS
authors.lastname: Eun
authors.forename: Yong Seok
authors.initials: YS
authors.lastname: Kim
authors.forename: Dong Soo
authors.initials: DS
authors.lastname: Han
authors.forename: Joo Hyun
authors.initials: JH
authors.lastname: Choi
authors.forename: A Reum
authors.initials: AR
authors.lastname: Lee
authors.forename: Yoon Kyung
authors.initials: YK
authors.lastname: Park
mesh_terms: D015153:Blotting, Western; D002070:Butadienes / Q000494:pharmacology; D018938:Caco-2 Cells; D002867:Chromones / Q000494:pharmacology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D007371:Interferon-gamma / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism* / Q000382:microbiology; D007780:Lacticaseibacillus casei; D008565:Membrane Proteins / Q000378:metabolism; D018613:Microscopy, Confocal; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009025:Morpholines / Q000494:pharmacology; D009570:Nitriles / Q000494:pharmacology; D010750:Phosphoproteins / Q000378:metabolism; D019936:Probiotics / Q000494:pharmacology*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D051195:Toll-Like Receptor 2 / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D062826:Zonula Occludens-1 Protein
chemical_list: D002070:Butadienes; D002867:Chromones; D007093:Imidazoles; D008565:Membrane Proteins; D009025:Morpholines; D009570:Nitriles; D010750:Phosphoproteins; D047428:Protein Kinase Inhibitors; D011725:Pyridines; C569042:TJP1 protein, human; C495342:TLR2 protein, human; D051195:Toll-Like Receptor 2; D014409:Tumor Necrosis Factor-alpha; C113580:U 0126; D062826:Zonula Occludens-1 Protein; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D007371:Interferon-gamma; D051057:Proto-Oncogene Proteins c-akt; D020928:Mitogen-Activated Protein Kinases; C093642:SB 203580