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Bacteroides fragilis enterotoxin upregulates heme oxygenase-1 in dendritic cells via reactive oxygen species-, mitogen-activated protein kinase-, and Nrf2-dependent pathway
- Bacteroides fragilis enterotoxin upregulates heme oxygenase-1 in dendritic cells via reactive oxygen species-, mitogen-activated protein kinase-, and Nrf2-dependent pathway
- Ko, Su Hyuk; Jeon, Jong Ik; Woo, Hyun Ae; Kim, Jung Mogg
- Ewha Authors
- SCOPUS Author ID
- Issue Date
- Journal Title
- WORLD JOURNAL OF GASTROENTEROLOGY
- WORLD JOURNAL OF GASTROENTEROLOGY vol. 26, no. 3, pp. 291 - 306
- Bacteroides fragilis enterotoxin; Dendritic cells; Heme oxygenase-1; Mitogen-activated protein kinases; Nrf2; Signaling
- BAISHIDENG PUBLISHING GROUP INC
- SCIE; SCOPUS
- Document Type
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- BACKGROUND Enterotoxigenic Bacteroides fragilis (ETBF) causes colitis and diarrhea, and is considered a candidate pathogen in inflammatory bowel diseases as well as colorectal cancers. These diseases are dependent on ETBF-secreted toxin (BFT). Dendritic cells (DCs) play an important role in directing the nature of adaptive immune responses to bacterial infection and heme oxygenase-1 (HO-1) is involved in the regulation of DC function. AIM To investigate the role of BFT in HO-1 expression in DCs. METHODS Murine DCs were generated from specific pathogen-free C57BL/6 and Nrf2(-/-) knockout mice. DCs were exposed to BFT, after which HO-1 expression and the related signaling factor activation were measured by quantitative RT-PCR, EMSA, fluorescent microscopy, immunoblot, and ELISA. RESULTS HO-1 expression was upregulated in DCs stimulated with BFT. Although BFT activated transcription factors such as NF-kappa B, AP-1, and Nrf2, activation of NF-kappa B and AP-1 was not involved in the induction of HO-1 expression in BFT-exposed DCs. Instead, upregulation of HO-1 expression was dependent on Nrf2 activation in DCs. Moreover, HO-1 expression via Nrf2 in DCs was regulated by mitogen-activated protein kinases such as ERK and p38. Furthermore, BFT enhanced the production of reactive oxygen species (ROS) and inhibition of ROS production resulted in a significant decrease of phospho-ERK, phospho-p38, Nrf2, and HO-1 expression. CONCLUSION These results suggest that signaling pathways involving ROS-mediated ERK and p38 mitogen-activated protein kinases-Nrf2 activation in DCs are required for HO-1 induction during exposure to ETBF-produced BFT.
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