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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.
- Source :
-
Clinical & Experimental Immunology . Oct2002, Vol. 130 Issue 1, p59-66. 8p. - Publication Year :
- 2002
-
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. [ABSTRACT FROM AUTHOR]
- Subjects :
- *ENTEROTOXINS
*CHEMOKINES
*EPITHELIAL cells
*NF-kappa B
Subjects
Details
- Language :
- English
- ISSN :
- 00099104
- Volume :
- 130
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Clinical & Experimental Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 7366698
- Full Text :
- https://doi.org/10.1046/j.1365-2249.2002.01921.x