Shi Tong, Liu Wen-zhong, Gao Fei, Xiao Shu-dong
Renji Hospital, Shanghai Second Medical University, Shanghai Institute of Digestive Disease, Shanghai 200001, China.
Zhonghua Yi Xue Za Zhi. 2003 Jan 25;83(2):133-6.
To investigate the role of nuclear factor kappaB (NF-kappaB) in the gastric inflammation induced by Helicobacter pylori (H. pylori).
SGC-7901 was transfected with IkappaB (NF-kappaB inhibitor gene) by electroporation, (beta)lacZ activity assay was used to examine transfected efficacy. Expression of IkappaB was assessed by Western-blot. Different concentration of live and heat-killed Hp (ATCC 43504) and supernatant of liquid culture were cocultured with SGC7901-IkappaB and its negative control SGC7901- neo. Activation of intracellular NF-kappaB was examined by electrophoretic mobility shift analyses (EMSA) and luciferase report gene assay at different time point. IL-8 levels were measured by ELISA at different time point.
IL-8 release was evident 4 hours after infection of SGC-7901-neo with H. pylori, and this effect was dose-time dependent. SGC-7901-IkappaB in which NF-kappaB has not been activated could not secret IL-8 after infection with H. pylori.
Secretion of IL-8 by gastric epithelial cell upon H pylori infection is dependent on activation of NF-kappaB.