Journal
LABORATORY INVESTIGATION
Volume 93, Issue 4, Pages 384-396Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/labinvest.2013.1
Keywords
AP-1; Bacteroides fragilis enterotoxin; intestinal epithelial cells; mitogen-activated protein kinase
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Funding
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology (MEST) [2010-0008594]
- NRF of Korea
- Korean Government (MEST) [2010-0029507]
- National Research Foundation of Korea [2010-0029507, 2010-0008594] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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. Laboratory Investigation (2013) 93, 384-396; doi:10.1038/labinvest.2013.1; published online 4 February 2013
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