Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김정목 | - |
dc.date.accessioned | 2018-03-23T08:56:00Z | - |
dc.date.available | 2018-03-23T08:56:00Z | - |
dc.date.issued | 2014-04 | - |
dc.identifier.citation | JOURNAL OF MOLECULAR MEDICINE-JMM; APR 2014, 92, 4, p411-p427 | en_US |
dc.identifier.issn | 0946-2716 | - |
dc.identifier.uri | https://link.springer.com/article/10.1007/s00109-013-1117-y | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/51666 | - |
dc.description.abstract | Clostridium difficile toxin A causes acute colitis associated with inflammatory cell infiltration and increased production of proinflammatory mediators. Although CX3CL1 (fractalkine) plays a role in chemoattracting monocytes/macrophages, NK cells, and T cells, little information is available on the regulated expression of CX3CL1 in response to toxin A stimulation. In this study, we investigated the role of C. difficile toxin A on CX3CL1 induction in intestinal epithelial cells. Stimulation of murine intestinal epithelial cells with toxin A resulted in the upregulation of CX3CL1. Expression of CX3CL1 was dependent on nuclear factor-kappaB (NF-kappa B) and I kappa B kinase (IKK) activation, while the suppression of activator protein-1 (AP-1) did not affect toxin A-induced CX3CL1 expression. Suppression of p38 mitogen-activated protein kinase (MAPK) significantly inhibited IKK-NF-kappa B signaling leading to CX3CL1 induction in C. difficile toxin A-stimulated cells. CX3CL1 was mainly secreted from the basolateral surfaces in toxin A-treated cells. Furthermore, inhibition of p38 activity attenuated the toxin A-induced upregulation of CX3CL1 in the mouse ileum in vivo. These results suggest that a pathway, including p38 MAPK, IKK, and NF-kappa B activation, is required for CX3CL1 induction in intestinal epithelial cells exposed to C. difficile toxin A and may regulate the development of intestinal inflammation induced by infection with toxigenic C. difficile. C. difficile toxin A causes colitis with inflammatory cell infiltration. CX3CL1 plays a role in chemoattracting immune cells. MAPK-NF-kappa B signaling is required for CX3CL1 induction in toxin A-exposed cells. CX3CL1 is mainly secreted from the basolateral surfaces. CX3CL1 may contribute to the regulation of toxigenic C. difficile infection. | en_US |
dc.description.sponsorship | Su Hyuk Ko and Jong Ik Jeon contributed equally to this work. We thank Dr. Martin F. Kagnoff for providing standard RNA for mouse β-actin. This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (MEST) (NRF-2013R1A1A2A-10004404) and a grant from the NRF of South Korea funded by the Korean Government (MEST) (MRC Program, NRF-2008-0062287). | en_US |
dc.language.iso | en | en_US |
dc.publisher | Springer | en_US |
dc.subject | Clostridium difficiletoxin A | en_US |
dc.subject | CX3CL1 | en_US |
dc.subject | Intestinal epithelial cells | en_US |
dc.subject | Mitogen-activated protein kinase | en_US |
dc.subject | Nuclear factor-kappaB | en_US |
dc.title | Mitogen-activated protein kinase/I kappa B kinase/NF-kappa B-dependent and AP-1-independent CX3CL1 expression in intestinal epithelial cells stimulated with Clostridium difficile toxin A | en_US |
dc.title.alternative | I kappa B kinase | en_US |
dc.type | Article | en_US |
dc.relation.volume | 92 | - |
dc.identifier.doi | 10.1007/s00109-013-1117-y | - |
dc.relation.page | 411-427 | - |
dc.relation.journal | JOURNAL OF MOLECULAR MEDICINE-JMM | - |
dc.contributor.googleauthor | Ko, Su Hyuk | - |
dc.contributor.googleauthor | Jeon, Jong Ik | - |
dc.contributor.googleauthor | Kim, Hyunah | - |
dc.contributor.googleauthor | Kim, Jung Mogg | - |
dc.contributor.googleauthor | Kim, Young-Jeon | - |
dc.contributor.googleauthor | Youn, Jeehee | - |
dc.relation.code | 2014033876 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jungmogg | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.