title: Cell wall fraction of Enterococcus hirae ameliorates TNF-alpha-induced barrier impairment in the human epithelial tight junction.
abstract: OBJECTIVE
  The evaluation of the effects of Enterococcus hirae, an intestinal bacterium in the adjacent mucosa (mucosal bacterium), on tumour necrosis factor-alpha (TNF-alpha)-induced barrier impairment in human epithelial Caco-2 cells.
  
  
  RESULTS
  The filter-grown Caco-2 monolayers were used as an intestinal epithelial model system. In Caco-2 cells, heat-killed E. hirae ATCC 9790(T) suppressed the TNF-alpha-induced barrier impairment and increase in interleukin-8 (IL-8) secretion, but lipase- and mutanolysin-treated E. hirae ATCC 9790(T) did not have these effects. It was demonstrated that lipoteichoic acid (LTA) from E. hirae ATCC 9790(T) is responsible for Caco-2 cells' recovery from TNF-alpha-induced impairments. In addition, Caco-2 cells had the same response to Toll-like receptor 2 (TLR2) ligand, Pam(3)Cys-Ser-(Lys)(4) as they did to LTA. Increased expression of zonula occludens-1 was observed by the addition of E. hirae ATCC 9790(T) to TNF-alpha-treated Caco-2 cells, and decreased expression of myosin light chain kinase was observed by the addition of LTA and Pam(3)Cys-Ser-(Lys)(4); this, in turn, led to barrier enforcement.
  
  
  CONCLUSIONS
  Enterococcus hirae ATCC 9790(T) cell wall fractions, such as LTA, protect against intestinal impairment by regulation of epithelial tight junction via TLR2 signalling.
  
  
  CONCLUSIONS
  Enterococcus hirae could be useful in the treatment of inflammatory bowel disease, as well as other intestinal disorders.
authors.affiliation: Graduate School of Biosphere Science, Hiroshima University, Hiroshima, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Miyauchi
authors.forename: H
authors.initials: H
authors.lastname: Morita
authors.forename: J
authors.initials: J
authors.lastname: Okuda
authors.forename: T
authors.initials: T
authors.lastname: Sashihara
authors.forename: M
authors.initials: M
authors.lastname: Shimizu
authors.forename: S
authors.initials: S
authors.lastname: Tanabe
mesh_terms: D018938:Caco-2 Cells; D002473:Cell Wall / Q000737:chemistry / Q000276:immunology*; D016983:Enterococcus / Q000737:chemistry / Q000276:immunology*; D004847:Epithelial Cells / Q000187:drug effects / Q000382:microbiology*; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis; D055666:Lipopeptides; D008070:Lipopolysaccharides / Q000276:immunology / Q000302:isolation & purification; D008565:Membrane Proteins / Q000096:biosynthesis; D009219:Myosin-Light-Chain Kinase / Q000096:biosynthesis; D010455:Peptides / Q000276:immunology; D010750:Phosphoproteins / Q000096:biosynthesis; D013682:Teichoic Acids / Q000276:immunology / Q000302:isolation & purification; D019108:Tight Junctions / Q000187:drug effects / Q000382:microbiology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*; D062826:Zonula Occludens-1 Protein
chemical_list: D016209:Interleukin-8; D055666:Lipopeptides; D008070:Lipopolysaccharides; D008565:Membrane Proteins; C508075:Pam(3)CSK(4) peptide; D010455:Peptides; D010750:Phosphoproteins; C569042:TJP1 protein, human; D013682:Teichoic Acids; D014409:Tumor Necrosis Factor-alpha; D062826:Zonula Occludens-1 Protein; C009900:lipoteichoic acid; D009219:Myosin-Light-Chain Kinase