Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
HELICOBACTER-PYLORI INDUCES AN INCREASE IN INOSITOL PHOSPHATES IN CULTURED EPITHELIAL-CELLS
Autore:
PUCCIARELLI MG; RUSCHKOWSKI S; TRUST TJ; FINLAY BB;
Indirizzi:
UNIV BRITISH COLUMBIA,BIOTECHNOL LAB,ROOM 237 VANCOUVER BC V6T 1Z3 CANADA UNIV BRITISH COLUMBIA,BIOTECHNOL LAB VANCOUVER BC V6T 1Z3 CANADA UNIV BRITISH COLUMBIA,DEPT MICROBIOL & IMMUNOL VANCOUVER BC V6T 1Z3 CANADA UNIV BRITISH COLUMBIA,DEPT BIOCHEM & MOLEC BIOL VANCOUVER BC V6T 1Z3 CANADA UNIV VICTORIA,DEPT BIOCHEM & MICROBIOL VICTORIA BC V8W 3P6 CANADA
Titolo Testata:
FEMS microbiology letters
fascicolo: 2-3, volume: 129, anno: 1995,
pagine: 293 - 299
SICI:
0378-1097(1995)129:2-3<293:HIAIII>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENTEROPATHOGENIC ESCHERICHIA-COLI; SIGNAL-TRANSDUCTION; PATHOGENESIS; GASTRITIS; PROTEINS; ENTRY;
Keywords:
HELICOBACTER PYLORI; SIGNAL TRANSDUCTION; INOSITOL PHOSPHATE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
16
Recensione:
Indirizzi per estratti:
Citazione:
M.G. Pucciarelli et al., "HELICOBACTER-PYLORI INDUCES AN INCREASE IN INOSITOL PHOSPHATES IN CULTURED EPITHELIAL-CELLS", FEMS microbiology letters, 129(2-3), 1995, pp. 293-299

Abstract

Helicobacter pylori is a bacterial pathogen of humans that infects the gastric mucosa. This infection has been associated with gastritis, peptic ulcers, and gastric carcinomas. Diverse in vitro studies have described efficient adherence of H. pylori to different types of epithelial cells. Because of its varied effects on host cells, we have analysed signal transduction events in H. pylori-infected epithelial cells. Our results show that H. pylori induces an increase in inositol phosphates in all cultured epithelial cells used, including HeLa, Henle 407,Hep-2, and the human gastric adenocarcinoma cell line AGS. Bacterial growth medium supernatants induce a similar response in the host cell. The increase in inositol phosphates is not related to redistribution of cytoskeletal proteins such as actin or cu-actinin nor tyrosine-phosphorylation of host cell proteins. The inositol phosphate increase is also observed in cells infected with low or non-adherent H. pylori mutants or mutants defective in the vacuolating toxin or urease holoenzyme. These results indicate that inositol phosphate release in H. pylori-infected cells is not dependent on bacterial adherence, and that a soluble bacterial factor, but not the vacuolating toxin or urease holoenzyme, mediates such an effect.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 05:10:27