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Am J Physiol Gastrointest Liver Physiol 281: G726-G734, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 3, G726-G734, September 2001

Helicobacter pylori lipopolysaccharide induces apoptosis of cultured guinea pig gastric mucosal cells

Tsukasa Kawahara, Shigetada Teshima, Yuki Kuwano, Ayuko Oka, Kyoichi Kishi, and Kazuhito Rokutan

Department of Nutrition, School of Medicine, University of Tokushima, Tokushima 770-8503, Japan

Helicobacter pylori lipopolysaccharide (LPS) is generally accepted as a low-toxicity virulence. Primary cultures of guinea pig gastric mucosal cells expressed the Toll-like receptor 4 and were sensitive to H. pylori LPS as well as Escherichia coli LPS. H. pylori LPS stimulated phosphorylation of transforming growth factor-beta -activated kinase 1 (TAK1), TAK1-binding protein 1 (TAB1), and c-Jun NH2-terminal kinase (JNK) 2. H. pylori LPS at >2.1 endotoxin unit/ml (>1 ng/ml) activated caspase-8, stimulated cytochrome c release from mitochondria, and subsequently activated caspases-9 and -3, leading to apoptosis. Epidermal growth factor blocked all of these apoptotic processes and inhibited apoptosis, whereas it did not modify the phosphorylation of TAK1, TAB1, and JNK2. A comparatively specific inhibitor of caspase-8 or -9 blocked apoptosis, whereas cytochrome c release was prevented only with a caspase-8-like inhibitor. Our results suggest that caspase-8 and mitochondria may play crucial roles in H. pylori LPS-induced apoptosis and that this accelerated apoptosis may be involved in abnormal cell turnover of H. pylori-infected gastric mucosa.

Toll-like receptor 4; caspase-8; mitochondria; epidermal growth factor; gastric pit cells


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