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• W2184529076 endingPage "G734" @default.
• W2184529076 startingPage "G726" @default.
• W2184529076 abstract "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 NH(2)-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." @default.
• W2184529076 created "2016-06-24" @default.
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• W2184529076 date "2001-09-01" @default.
• W2184529076 modified "2023-09-27" @default.
• W2184529076 title "<i>Helicobacter pylori</i>lipopolysaccharide induces apoptosis of cultured guinea pig gastric mucosal cells" @default.
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• W2184529076 doi "https://doi.org/10.1152/ajpgi.2001.281.3.g726" @default.
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