Bacteroides fragilis enterotoxin upregulates lipocalin-2 expression in intestinal epithelial cells
| Autor: | Jireh Jung, Young Jeon Kim, Jung Mogg Kim, Su Hyuk Ko, Joo Sung Kim, Do Young Yoo |
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| Rok vydání: | 2013 |
| Předmět: |
MAP Kinase Signaling System
p38 mitogen-activated protein kinases Bacterial Toxins Enterotoxin Lipocalin Pathology and Forensic Medicine Microbiology Lipocalin-2 Downregulation and upregulation Proto-Oncogene Proteins Humans Intestinal Mucosa Molecular Biology biology Kinase NF-kappa B Metalloendopeptidases Epithelial Cells Cell Biology biology.organism_classification Lipocalins Up-Regulation Transcription Factor AP-1 Mitogen-activated protein kinase biology.protein Bacteroides fragilis Signal transduction HT29 Cells Acute-Phase Proteins |
| Zdroj: | Laboratory Investigation. 93:384-396 |
| ISSN: | 0023-6837 |
| Popis: | Enterotoxigenic Bacteroides fragilis (ETBF) produces an ≈ 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 β-defensin (hBD)-2 expression. The upregulation of Lcn-2 was dependent on AP-1 but not on NF-κB 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. |
| Databáze: | OpenAIRE |
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