Intestinal Epithelial Cells Exposed to Bacteroides fragilis Enterotoxin Regulate NF-κB Activation and Inflammatory Responses through β-Catenin Expression
- Authors
- Jeon, Jong Ik; Ko, Su Hyuk; Kim, Jung Mogg
- Issue Date
- Nov-2019
- Publisher
- AMER SOC MICROBIOLOGY
- Keywords
- Bacteroides fragilis; enterotoxin; intestinal epithelial cells; NK-κB; β-catenin
- Citation
- INFECTION AND IMMUNITY, v.87, no.11, pp.1 - 16
- Indexed
- SCIE
SCOPUS
- Journal Title
- INFECTION AND IMMUNITY
- Volume
- 87
- Number
- 11
- Start Page
- 1
- End Page
- 16
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/146825
- DOI
- 10.1128/IAI.00312-19
- ISSN
- 0019-9567
- 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 beta-catenin signaling is reported to be associated with inflammatory responses and BFT is known to cleave E-cadherin linked with beta-catenin, little is known about the beta-catenin-mediated regulation of inflammation in ETBF infection. This study was conducted to investigate the role of beta-catenin as a cellular signaling intermediate in the induction of proinflammatory responses to stimulation of intestinal epithelial cells with BFT. Expression of beta-catenin in intestinal epithelial cells was reduced relatively early after stimulation with BFT and then recovered to normal levels relatively late after stimulation. In contrast, phosphorylation of beta-catenin in BFT-exposed cells occurred at high levels early in stimulation and decreased as time passed. Concurrently, late after stimulation the nuclear levels of beta-catenin were relatively higher than those early after stimulation. Suppression of beta-catenin resulted in increased NF-kappa B activity and interleukin-8 (IL-8) expression in BFT-stimulated cells. However, suppression or enhancement of beta-catenin expression neither altered the phosphorylated I kappa B kinase alpha/beta complex nor activated activator protein 1 signals. Furthermore, inhibition of glycogen synthase kinase 3 beta was associated with increased beta-catenin expression and attenuated NF-kappa B activity and IL-8 expression in BFT-exposed cells. These findings suggest the negative regulation of NF-kappa B-mediated inflammatory responses by beta-catenin in intestinal epithelial cells stimulated with BFT, resulting in attenuation of acute inflammation in ETBF infection.
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