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Am J Physiol Gastrointest Liver Physiol 281: G735-G742, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 3, G735-G742, September 2001

Gastrin induces CXC chemokine expression in gastric epithelial cells through activation of NF-kappa B

Shintaro Hiraoka1, Yoshiji Miyazaki1, Shinji Kitamura1, Miyuki Toyota1, Tatsuya Kiyohara1, Yasuhisa Shinomura1, Naofumi Mukaida2, and Yuji Matsuzawa1

1 Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 565-0871 Osaka; and 2 Department of Molecular Pharmacology, Cancer Research Institute, Kanazawa University, 920-0934 Kanazawa, Japan

Although hypergastrinemia is frequently observed in individuals with a chronic Helicobacter pylori infection, its pathophysiological significance in gastric mucosal inflammation is unclear. The present study was designed to determine if gastrin induces the expression of CXC chemokines in gastric epithelial cells. Human and rat gastric epithelial cells, transfected with gastrin receptor, were stimulated with gastrin. The expression of mRNAs for human interleukin-8 (IL-8) and rat cytokine-induced neutrophil chemoattractant-1 and release of human IL-8 protein were then determined by Northern blot analysis and ELISA, respectively. Gastrin not only induced the expression of mRNAs for these chemokines but also stimulated IL-8 protein release. A luciferase assay using IL-8 promoter genes showed that nuclear factor (NF)-kappa B is absolutely required and activator protein-1 (AP-1) is partly required for the maximum induction of IL-8 by gastrin. An electrophoretic mobility shift assay revealed that gastrin is capable of activating both NF-kappa B and AP-1. In addition, the inhibition of NF-kappa B abrogated gastrin-induced chemokine expression. These results suggest that gastrin is capable of upregulating CXC chemokines in gastric epithelial cells and therefore may contribute to the progression of the inflammatory process in the stomach.

mucosa; inflammation; chemokines; transcription factors


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