Publication Database

TcpC protein from E. coli Nissle improves epithelial barrier function involving PKCζ and ERK1/2 signaling in HT-29/B6 cells (2014)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Hering, N A

Richter, J F

Fromm, A

Wieser, A

Hartmann, S (WE 6)

Günzel, D

Bücker, R

Fromm, M

Schulzke, J D

Troeger, H

Quelle

Mucosal immunology : official journal of the Society for Mucosal Immunology

Bandzählung: 7

Heftzählung: 2

Seiten: 369 – 378

ISSN: 1933-0219

Sprache

Englisch

Verweise

DOI: 10.1038/mi.2013.55

Pubmed: 23900194

Kontakt

Institut für Immunologie

Robert-von-Ostertag-Str. 7-13
14163 Berlin
+49 30 838 51834
immunologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

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.