A ${sim}20;kDa$ heat-labile toxin produced by enterotoxigenic Bacteroides fragilis (BFT) induces the expression of CXC chemokines from intestinal epithelial cells. To elucidate signaling pathway involved in chemokine expression of BFT stimulated-epithelial cells, we assessed the activation of nuc1ear factor-kappa B (NF-${kappa}B$) by BFT-stimulated human intestinal epithelial cells. The human intestinal epithelial HT-29 cells were incubated with purified BFT. NF-${kappa}B$ signal was detected by electrophoretic mobility shift assay and $I{kappa}B$ signals were assessed by immunoblots. Chemokine production was measured by ELISA and mRNA levels were assessed by quantitative RT-PCR. BFT stimulation increased NF-${kappa}B$ signals in HT-29 cells. In contrast, $I{kappa}B{alpha}$ and $I{kappa}B{varepsilon}$ signals were decreased upon BFT stimulation. The subunits involved in the rapid activation of NF-${kappa}B$ were p65 and p50. Transfection of dominant-negative $I{kappa}B{alpha}$ or $I{kappa}B$ kinase (IKK)${eta}$ plasmid inhibited an up-regulated transcription of downstream target gene (interleukin-8) of NF-${kappa}B$. In addition, a blockage of NF-${kappa}B$ activation by MG-132 resulted in down-regulated gene expression of CXC chemokines such as interleukin-8 and growth-related oncogene-${alpha}$ in BFT-stimulated HT-29 cells. These results indicate that NF-${kappa}B$ may function as a central regulator of chemokine gene expression in BFT-stimulated intestinal epithelial cells.