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dc.contributor.author우현애-
dc.date.accessioned2020-02-07T16:30:06Z-
dc.date.available2020-02-07T16:30:06Z-
dc.date.issued2020-
dc.identifier.issn1007-9327-
dc.identifier.issn2219-2840-
dc.identifier.otherOAK-26437-
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/253310-
dc.description.abstractBACKGROUND 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.-
dc.languageEnglish-
dc.publisherBAISHIDENG PUBLISHING GROUP INC-
dc.subjectBacteroides fragilis enterotoxin-
dc.subjectDendritic cells-
dc.subjectHeme oxygenase-1-
dc.subjectMitogen-activated protein kinases-
dc.subjectNrf2-
dc.subjectSignaling-
dc.titleBacteroides fragilis enterotoxin upregulates heme oxygenase-1 in dendritic cells via reactive oxygen species-, mitogen-activated protein kinase-, and Nrf2-dependent pathway-
dc.typeArticle-
dc.relation.issue3-
dc.relation.volume26-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage291-
dc.relation.lastpage306-
dc.relation.journaltitleWORLD JOURNAL OF GASTROENTEROLOGY-
dc.identifier.doi10.3748/wjg.v26.i3.291-
dc.identifier.wosidWOS:000536254500003-
dc.identifier.scopusid2-s2.0-85078337297-
dc.author.googleKo, Su Hyuk-
dc.author.googleJeon, Jong Ik-
dc.author.googleWoo, Hyun Ae-
dc.author.googleKim, Jung Mogg-
dc.contributor.scopusid우현애(8068619500)-
dc.date.modifydate20200715111627-
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약학대학 > 약학과 > Journal papers
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