Bacteroides fragilisEnterotoxin Induces Sulfiredoxin-1 Expression in Intestinal Epithelial Cell Lines Through a Mitogen-Activated Protein Kinases- and Nrf2-Dependent Pathway, Leading to the Suppression of Apoptosisopen access
- Authors
- Jeon, Jong Ik; Choi, Jun Ho; Lee, Keun Hwa; Kim, Jung Mogg
- Issue Date
- Aug-2020
- Publisher
- MDPI
- Keywords
- Bacteroides fragilis; enterotoxin; intestinal epithelial cells; sulfiredoxin-1
- Citation
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.21, no.15, pp.1 - 17
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
- Volume
- 21
- Number
- 15
- Start Page
- 1
- End Page
- 17
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/145298
- DOI
- 10.3390/ijms21155383
- ISSN
- 1661-6596
- Abstract
- EnterotoxigenicBacteroides fragilisis a causative agent of colitis and secrets enterotoxin (BFT), leading to the disease. Sulfiredoxin (Srx)-1 serves to protect from oxidative damages. Although BFT can generate reactive oxygen species in intestinal epithelial cells (IECs), no Srx-1 expression has been reported in ETBF infection. In this study, we explored the effects of ETBF-produced BFT on Srx-1 induction in IECs. Treatment of IECs with BFT resulted in increased expression of Srx-1 in a time-dependent manner. BFT treatment also activated transcriptional signals including Nrf2, AP-1 and NF-kappa B, and the Srx-1 induction was dependent on the activation of Nrf2 signals. Nrf2 activation was assessed using immunoblot and Nrf2-DNA binding activity and the specificity was confirmed by supershift and competition assays. Suppression of NF-kappa B or AP-1 signals did not affect the upregulation of Srx-1 expression. Nrf2-dependent Srx-1 expression was associated with the activation of p38 mitogen-activated protein kinases (MAPKs) in IECs. Furthermore, suppression of Srx-1 significantly enhanced apoptosis while overexpression of Srx-1 significantly attenuated apoptosis during exposure to BFT. These results imply that a signaling cascade involving p38 and Nrf2 is essential for Srx-1 upregulation in IECs stimulated with BFT. Following this upregulation, Srx-1 may control the apoptosis in BFT-exposed IECs.
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