Bacteroides fragilis Enterotoxin Upregulates Heme Oxygenase-1 in Intestinal Epithelial Cells via a Mitogen-Activated Protein Kinase- and NF-kappa B-Dependent Pathway, Leading to Modulation of Apoptosis
DC Field | Value | Language |
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dc.contributor.author | Ko, Su Hyuk | - |
dc.contributor.author | Rho, Da Jeong | - |
dc.contributor.author | Jeon, Jong Ik | - |
dc.contributor.author | Kim, Young-Jeon | - |
dc.contributor.author | Woo, Hyun Ae | - |
dc.contributor.author | Lee, Yun Kyung | - |
dc.contributor.author | Kim, Jung Mogg | - |
dc.date.accessioned | 2022-07-15T07:15:23Z | - |
dc.date.available | 2022-07-15T07:15:23Z | - |
dc.date.created | 2021-05-12 | - |
dc.date.issued | 2016-09 | - |
dc.identifier.issn | 0019-9567 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/154020 | - |
dc.description.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 expression of heme oxygenase-1 (HO-1) is associated with regulation of inflammatory responses, little is known about HO-1 induction in ETBF infection. This study was conducted to investigate the effect of BFT on HO-1 expression in intestinal epithelial cells. Stimulation of intestinal epithelial cells with BFT resulted in upregulated expression of HO-1. BFT activated transcription factors such as NF-kappa B, AP-1, and Nrf2 in intestinal epithelial cells. Upregulation of HO-1 in intestinal epithelial cells was dependent on activated I kappa B kinase (IKK)-NF-kappa B signals. However, suppression of Nrf2 or AP-1 signals in intestinal epithelial cells did not result in significant attenuation of BFT-induced HO-1 expression. HO-1 induction via IKK-NF-kappa B in intestinal epithelial cells was regulated by p38 mitogen-activated protein kinases (MAPKs). Furthermore, suppression of HO-1 activity led to increased apoptosis in BFT-stimulated epithelial cells. These results suggest that a signaling pathway involving p38 MAPK-IKK-NF-kappa B in intestinal epithelial cells is required for HO-1 induction during exposure to BFT. Following this induction, increased HO-1 expression may regulate the apoptotic process in responses to BFT stimulation. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC MICROBIOLOGY | - |
dc.title | Bacteroides fragilis Enterotoxin Upregulates Heme Oxygenase-1 in Intestinal Epithelial Cells via a Mitogen-Activated Protein Kinase- and NF-kappa B-Dependent Pathway, Leading to Modulation of Apoptosis | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Jung Mogg | - |
dc.identifier.doi | 10.1128/IAI.00191-16 | - |
dc.identifier.scopusid | 2-s2.0-84984852086 | - |
dc.identifier.wosid | 000382320300014 | - |
dc.identifier.bibliographicCitation | INFECTION AND IMMUNITY, v.84, no.9, pp.2541 - 2554 | - |
dc.relation.isPartOf | INFECTION AND IMMUNITY | - |
dc.citation.title | INFECTION AND IMMUNITY | - |
dc.citation.volume | 84 | - |
dc.citation.number | 9 | - |
dc.citation.startPage | 2541 | - |
dc.citation.endPage | 2554 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Immunology | - |
dc.relation.journalResearchArea | Infectious Diseases | - |
dc.relation.journalWebOfScienceCategory | Immunology | - |
dc.relation.journalWebOfScienceCategory | Infectious Diseases | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | PROMOTES | - |
dc.subject.keywordPlus | NRF2 | - |
dc.subject.keywordPlus | SECRETION | - |
dc.subject.keywordPlus | COMMENSAL | - |
dc.subject.keywordPlus | COLITIS | - |
dc.subject.keywordPlus | INJURY | - |
dc.subject.keywordPlus | ALPHA | - |
dc.subject.keywordPlus | MAPK | - |
dc.identifier.url | https://journals.asm.org/doi/10.1128/IAI.00191-16 | - |
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