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J Bacteriol Virol. 2004 Mar;34(1):83-90. Korean. Original Article.
Kim JM , Oh YK , Lee Y , Kim YJ .
Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Korea. jungmogg@hanyang.ac.kr
Department of Microbiology and Institute of Medical Research, Pochon CHA University College of Medicine, Korea.
Department of Biotechnology, Joongbu University, Korea.
Abstract

A ~20 kDa heat-labile toxin (BFT) produced by enterotoxigenic B. fragilis induces chemokine responses that are associated with mucosal inflammation. In the present study, we assessed whether the activation of mitogen-activated protein kinase (MAPK) affects the levels of IL-8 and MCP-1 produced by BFT stimulation in human epithelial HT-29 cells. Human intestinal epithelial HT-29 cell lines were incubated with purified BFT. MAPK and AP-1 in HT-29 cells were measured by Western blot and luciferase assay, respectively. The expression of chemokines such as IL-8 and MCP-1 were determined by quantitative RT-PCR, ELISA, and luciferase assay. BFT stimulation activated MAPK such as ERK1/2 and p38 in HT-29 cells. Treatment with MAPK inhibitors attenuated BFT-induced expression of IL-8 and MCP-1. Transfection with mutant genes for Ras or c-Jun did not only suppressed AP-1 reporter genes, but also inhibited BFT-induced expression of IL-8 and MCP-1 reporter genes. These results suggest that Ras and MAPK cascade may act as the upstream signaling for the activation of AP-1, which induce chemokine expression in BFT-stimulated intestinal epithelial cells.

Copyright © 2019. Korean Association of Medical Journal Editors.