| Autor: |
Klapproth, Jan-Michael Axel, Sasaki, Maiko, Sitaraman, Shanti V., Alpern, Joel A., Akyildiz, Adil, Theiss, Arianne L., Nusrat, Asma |
| Předmět: |
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| Zdroj: |
FASEB Journal; Apr2007, Vol. 21 Issue 5, pA585-A585, 1/5p |
| Abstrakt: |
Introduction: The apical junctional complex (AJC) regulates epithelial barrier function and is compromised in inflammatory bowel disease (IBD). Hypothesis: Disease specific E. coli regulate epithelial barrier function in IBD. Material and methods: Invasive E. coli were isolated from tissue of Crohn's disease (CD), ulcerative colitis (UC), and normal control patients. Epithelial barrier function was determined by transepithelial resistance (TER) and confocal microscopy of model intestinal epithelial cell line, Caco2. Macrophage cultures co-cultured with specific E. coli were analyzed for TNF-a production. Results: Epithelial invasion indices for E. coli from CD were significantly higher in comparison to UC, and highest from inflamed CD tissue. IBD E. coli strains lead to a 79% decrease in TER, redistribution of F-actin and displacement of AJC proteins from the lateral membrane. Infection of macrophage cultures with IBD E. coli induced very high concentrations of TNF-α, especially for E. coli from inflamed CD tissue. Summary: Invasive E. coli from patients with IBD regulate barrier function through redistribution and disassembly of the AJC. IBD specific strains also induce expression of high TNF-α concentrations in macrophage cultures. Conclusion: We propose a mechanism by which IBD specific invasive E. coli breach epithelial integrity, gain access to mucosal macrophages, induce high concentrations of TNF-α, thereby further exacerbating loss of epithelial barrier function. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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