<i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release
<i>Bacteroides fragilis</i> enterotoxin (BFT) produced by enterotoxigenic <i>B. fragilis</i> (ETBF) causes colonic inflammation. BFT initially contacts intestinal epithelial cells (IECs) and affects the intestinal barrier. Although molecular components of the gut epithelial b...
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oai:doaj.org-article:91f76811547f4221a4413eb4b8728d802021-11-11T17:15:25Z<i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release10.3390/ijms2221118171422-00671661-6596https://doaj.org/article/91f76811547f4221a4413eb4b8728d802021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11817https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067<i>Bacteroides fragilis</i> enterotoxin (BFT) produced by enterotoxigenic <i>B. fragilis</i> (ETBF) causes colonic inflammation. BFT initially contacts intestinal epithelial cells (IECs) and affects the intestinal barrier. Although molecular components of the gut epithelial barrier such as metalloproteinase-7 (MMP-7) and syndecan-2 are known to be associated with inflammation, little has been reported about MMP-7 expression and syndecan-2 shedding in response to ETBF infection. This study explores the role of BFT in MMP-7 induction and syndecan-2 release in IECs. Stimulating IECs with BFT led to the induction of MMP-7 and the activation of transcription factors such as NF-κB and AP-1. MMP-7 upregulation was not affected by NF-κB, but it was related to AP-1 activation. In BFT-exposed IECs, syndecan-2 release was observed in a time- and concentration-dependent manner. MMP-7 suppression was associated with a reduction in syndecan-2 release. In addition, suppression of ERK, one of the mitogen-activated protein kinases (MAPKs), inhibited AP-1 activity and MMP-7 expression. Furthermore, the suppression of AP-1 and ERK activity was related to the attenuation of syndecan-2 release. These results suggest that a signaling cascade comprising ERK and AP-1 activation in IECs is involved in MMP-7 upregulation and syndecan-2 release during exposure to BFT.Jong Ik JeonKeun Hwa LeeJung Mogg KimMDPI AGarticle<i>Bacteroides fragilis</i>enterotoxinIECsMMP-7syndecan-2Biology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11817, p 11817 (2021) |
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<i>Bacteroides fragilis</i> enterotoxin IECs MMP-7 syndecan-2 Biology (General) QH301-705.5 Chemistry QD1-999 |
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<i>Bacteroides fragilis</i> enterotoxin IECs MMP-7 syndecan-2 Biology (General) QH301-705.5 Chemistry QD1-999 Jong Ik Jeon Keun Hwa Lee Jung Mogg Kim <i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release |
description |
<i>Bacteroides fragilis</i> enterotoxin (BFT) produced by enterotoxigenic <i>B. fragilis</i> (ETBF) causes colonic inflammation. BFT initially contacts intestinal epithelial cells (IECs) and affects the intestinal barrier. Although molecular components of the gut epithelial barrier such as metalloproteinase-7 (MMP-7) and syndecan-2 are known to be associated with inflammation, little has been reported about MMP-7 expression and syndecan-2 shedding in response to ETBF infection. This study explores the role of BFT in MMP-7 induction and syndecan-2 release in IECs. Stimulating IECs with BFT led to the induction of MMP-7 and the activation of transcription factors such as NF-κB and AP-1. MMP-7 upregulation was not affected by NF-κB, but it was related to AP-1 activation. In BFT-exposed IECs, syndecan-2 release was observed in a time- and concentration-dependent manner. MMP-7 suppression was associated with a reduction in syndecan-2 release. In addition, suppression of ERK, one of the mitogen-activated protein kinases (MAPKs), inhibited AP-1 activity and MMP-7 expression. Furthermore, the suppression of AP-1 and ERK activity was related to the attenuation of syndecan-2 release. These results suggest that a signaling cascade comprising ERK and AP-1 activation in IECs is involved in MMP-7 upregulation and syndecan-2 release during exposure to BFT. |
format |
article |
author |
Jong Ik Jeon Keun Hwa Lee Jung Mogg Kim |
author_facet |
Jong Ik Jeon Keun Hwa Lee Jung Mogg Kim |
author_sort |
Jong Ik Jeon |
title |
<i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release |
title_short |
<i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release |
title_full |
<i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release |
title_fullStr |
<i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release |
title_full_unstemmed |
<i>Bacteroides fragilis</i> Enterotoxin Upregulates Matrix Metalloproteinase-7 Expression through MAPK and AP-1 Activation in Intestinal Epithelial Cells, Leading to Syndecan-2 Release |
title_sort |
<i>bacteroides fragilis</i> enterotoxin upregulates matrix metalloproteinase-7 expression through mapk and ap-1 activation in intestinal epithelial cells, leading to syndecan-2 release |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/91f76811547f4221a4413eb4b8728d80 |
work_keys_str_mv |
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