Open AccessBacteroides fragilisEnterotoxin Induces Human β-Defensin-2 Expression in Intestinal Epithelial Cells via a Mitogen-Activated Protein Kinase/IκB Kinase/NF-κB-Dependent Pathway
Author(s) -
Young Mee Yoon,
Jin Young Lee,
Doyoung Yoo,
Young Suk Sim,
Young Jeon Kim,
YuKyoung Oh,
Jae Seon Kang,
Sunil Kim,
Sang Woo Kim,
Jung Mogg Kim
Publication year - 2010
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00118-10
Subject(s) - biology , bacteroides fragilis , p38 mitogen activated protein kinases , defensin , protein kinase a , kinase , mapk/erk pathway , small interfering rna , iκb kinase , mitogen activated protein kinase , nf κb , heat stable enterotoxin , microbiology and biotechnology , signal transduction , transfection , cell culture , enterotoxin , gene , biochemistry , escherichia coli , antimicrobial , antibiotics , genetics
EnterotoxigenicBacteroides fragilis (ETBF) produces an approximately 20-kDa heat-labile enterotoxin (BFT) that plays an essential role in mucosal inflammation. Although spontaneous disappearance of ETBF infection is common, little information is available on regulated expression of antibacterial factors in response to BFT stimulation. This study investigates the role of BFT in human β-defensin 2 (hBD-2) induction from intestinal epithelial cells. Stimulation of HT-29 and Caco-2 intestinal epithelial cell lines with BFT resulted in the induction of hBD-2. Activation of a reporter gene for hBD-2 was dependent on the presence of NF-κB binding sites. In contrast, suppression of AP-1 did not affect hBD-2 expression in BFT-stimulated cells. Inhibition of p38 mitogen-activated protein kinase (MAPK) using SB203580 and small interfering RNA (siRNA) transfection resulted in a significant reduction in BFT-induced IκB kinase (IKK)/NF-κB activation and hBD-2 expression. Our results suggest that a pathway including p38 MAPK, IKK, and NF-κB activation is required for hBD-2 induction in intestinal epithelial cells exposed to BFT, and may be involved in the host defense following infection with ETBF.