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- Title
Nuclear factor-kappa B activation pathway in intestinal epithelial cells is a major regulator of chemokine gene expression and neutrophil migration induced by Bacteroides fragilis enterotoxin.
- Authors
KIM, J. M.; CHO, S. J.; OH, Y.-K.; JUNG, H.-Y.; KIM, Y.-J.
- Abstract
SUMMARY Although intestinal epithelial cells are known to up-regulate the expression of several chemokine genes in response to the stimulation with B. fragilis enterotoxin (BFT), there has been little understanding on the cellular mechanisms of BFT-induced mucosal inflammation. To test whether nuclear transcriptional factor-kappa B (NF-κB) is involved in the process, we stimulated intestinal epithelial cells with BFT, and evaluated the signalling NF-κB pathways. BFT increased signals of NF-κB in HT-29 and T84 epithelial cell lines as well as primary human colon epithelial cells. NF-κB molecules activated by BFT stimulation were composed of p65 and p50 heterodimers. In contrast, BFT decreased the signals of IκBα and IκBℇ, as assessed by immunoblot. Super-repressors of IκBα, IκB kinase (IKK)β, and NF-κB inducing kinase (NIK) inhibited an up-regulated transcription of downstream target gene (CXCL8) of NF-κB. Moreover, blocking the activation of NF-κB by MG-132 or antisense p50 oligonucleotide transfection resulted in down-regulated expression of chemokines such as CXCL1, CXCL8, and CCL2 in BFT-stimulated HT-29 cells. In addition, NF-κB inhibition suppressed the BFT-induced neutrophil transepithelial migration in T84 cells. These results indicate that NF-κB can be a central regulator of chemokine gene expression in BFT-stimulated intestinal epithelial cells and may be an important regulator of neutrophil migration.
- Subjects
ENTEROTOXINS; CHEMOKINES; EPITHELIAL cells; NF-kappa B
- Publication
Clinical & Experimental Immunology, 2002, Vol 130, Issue 1, p59
- ISSN
0009-9104
- Publication type
Article
- DOI
10.1046/j.1365-2249.2002.01921.x