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TcpC protein from E. coli Nissle improves epithelial barrier function involving PKCζ and ERK1/2 signaling in HT-29/B6 cells.

Abstract
The probiotic Escherichia coli Nissle 1917 (EcN) is widely used to maintain remission in ulcerative colitis. This is thought to be mediated by various immunomodulatory and barrier-stabilizing effects in the intestine. In this study, the mechanisms of barrier modulation by EcN were studied in the human epithelial HT-29/B6 cell culture model.EcN supernatant increased transepithelial resistance (TER) and reduced permeability to mannitol because of sealing of the paracellular passage pathway as revealed by two-path impedance spectroscopy. This increase in TER was attributed to the TcpC protein of EcN. TcpC induced protein kinase C-ζ (PKCζ) and extracellular-signal-regulated kinase 1/2 (ERK1/2) phosphorylation, which in turn resulted in upregulation of the barrier-forming tight junction protein claudin-14. By specific silencing of protein expression by small interfering RNA (siRNA), the sealing function of claudin-14 was confirmed. In conclusion, the TcpC protein of EcN affects innate immunity by improving intestinal barrier function through upregulation of claudin-14 via PKCζ and ERK1/2 signaling.
AuthorsN A Hering, J F Richter, A Fromm, A Wieser, S Hartmann, D Günzel, R Bücker, M Fromm, J D Schulzke, H Troeger
JournalMucosal immunology (Mucosal Immunol) Vol. 7 Issue 2 Pg. 369-78 (Mar 2014) ISSN: 1935-3456 [Electronic] United States
PMID23900194 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Claudins
  • Escherichia coli Proteins
  • TcpC protein, E coli
  • Virulence Factors
  • Protein Kinase C
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • claudin 14
Topics
  • Animals
  • Animals, Newborn
  • Cell Line
  • Claudins (metabolism)
  • Epithelial Cells (drug effects, metabolism)
  • Escherichia coli (metabolism)
  • Escherichia coli Proteins (genetics, metabolism, pharmacology)
  • Gene Knockout Techniques
  • HT29 Cells
  • Humans
  • Mitogen-Activated Protein Kinase 1 (metabolism)
  • Mitogen-Activated Protein Kinase 3 (metabolism)
  • Mucous Membrane (drug effects, immunology, metabolism)
  • Permeability
  • Phosphorylation (drug effects)
  • Protein Kinase C (metabolism)
  • Signal Transduction (drug effects)
  • Swine
  • Virulence Factors (genetics, metabolism, pharmacology)

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