26 0

Bacteroides fragilis Enterotoxin Upregulates Heme Oxygenase-1 in Intestinal Epithelial Cells via a Mitogen-Activated Protein Kinase- and NF-kappa B-Dependent Pathway, Leading to Modulation of Apoptosis

Title
Bacteroides fragilis Enterotoxin Upregulates Heme Oxygenase-1 in Intestinal Epithelial Cells via a Mitogen-Activated Protein Kinase- and NF-kappa B-Dependent Pathway, Leading to Modulation of Apoptosis
Author
고수혁
Keywords
INDUCED COLITIS; EXPRESSION; INDUCTION; MICE; PROMOTES; NRF2; MACROPHAGES; SECRETION; MONOCYTES; COMMENSAL
Issue Date
2016-05
Publisher
AMER SOC MICROBIOLOGY
Citation
INFECTION AND IMMUNITY, v. 84, NO 9, Page. 2541-2554
Abstract
The Bacteroides fragilis enterotoxin (BFT), a virulence factor of enterotoxigenic B. fragilis (ETBF), interacts with intestinal epithelial cells and can provoke signals that induce mucosal inflammation. Although expression of heme oxygenase-1 (HO-1) is associated with regulation of inflammatory responses, little is known about HO-1 induction in ETBF infection. This study was conducted to investigate the effect of BFT on HO-1 expression in intestinal epithelial cells. Stimulation of intestinal epithelial cells with BFT resulted in upregulated expression of HO-1. BFT activated transcription factors such as NF-kappa B, AP-1, and Nrf2 in intestinal epithelial cells. Upregulation of HO-1 in intestinal epithelial cells was dependent on activated I kappa B kinase (IKK)-NF-kappa B signals. However, suppression of Nrf2 or AP-1 signals in intestinal epithelial cells did not result in significant attenuation of BFT-induced HO-1 expression. HO-1 induction via IKK-NF-kappa B in intestinal epithelial cells was regulated by p38 mitogen-activated protein kinases (MAPKs). Furthermore, suppression of HO-1 activity led to increased apoptosis in BFT-stimulated epithelial cells. These results suggest that a signaling pathway involving p38 MAPK-IKK-NF-kappa B in intestinal epithelial cells is required for HO-1 induction during exposure to BFT. Following this induction, increased HO-1 expression may regulate the apoptotic process in responses to BFT stimulation.
URI
http://iai.asm.org/content/84/9/2541http://hdl.handle.net/20.500.11754/68063
ISSN
0019-9567; 1098-5522
DOI
10.1128/IAI.00191-16
Appears in Collections:
RESEARCH INSTITUTE[S](부설연구소) > ETC
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE