Bacteroides fragilis enterotoxin upregulates lipocalin-2 expression in intestinal epithelial cells
- Authors
- Yoo, Do Young; Ko, Su Hyuk; Jung, Jireh; Kim, Young-Jeon; Kim, Joo Sung; Kim, Jung Mogg
- Issue Date
- Apr-2013
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- AP-1; Bacteroides fragilis enterotoxin; intestinal epithelial cells; mitogen-activated protein kinase
- Citation
- LABORATORY INVESTIGATION, v.93, no.4, pp.384 - 396
- Indexed
- SCIE
SCOPUS
- Journal Title
- LABORATORY INVESTIGATION
- Volume
- 93
- Number
- 4
- Start Page
- 384
- End Page
- 396
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/163057
- DOI
- 10.1038/labinvest.2013.1
- ISSN
- 0023-6837
- Abstract
- Enterotoxigenic Bacteroides fragilis (ETBF) produces an similar to 20 kDa B. fragilis enterotoxin (BFT), which plays an essential role in mucosal inflammation. Lipocalin (Lcn)-2, a siderophore-binding antimicrobial protein, is critical for control of bacterial infection; however, expression of Lcn-2 in BFT-exposed intestinal epithelial cells has not been elucidated. In the present study, stimulation of human intestinal epithelial cells with BFT resulted in the upregulation of Lcn-2 expression that was a relatively late response of intestinal epithelial cells compared with human beta-defensin (hBD)-2 expression. The upregulation of Lcn-2 was dependent on AP-1 but not on NF-kappa B signaling. Lcn-2 induction via AP-1 was regulated by mitogen-activated protein kinases (MAPKs) including ERK and p38. Lcn-2 was secreted from the apical and basolateral surfaces in BFT-treated cells. These results suggest that a signaling pathway involving MAPKs and AP-1 is required for Lcn-2 induction in intestinal epithelial cells exposed to BFT, after which the secreted Lcn-2 may facilitate antimicrobial activity within ETBF-infected mucosa.
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