Helicobacter pylori cag pathogenicity island is associated with enhanced Interleukin-8 expression in human gastric mucosa

Citation
B. Orsini et al., Helicobacter pylori cag pathogenicity island is associated with enhanced Interleukin-8 expression in human gastric mucosa, DIG LIVER D, 32(6), 2000, pp. 458-467
Citations number
51
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
DIGESTIVE AND LIVER DISEASE
ISSN journal
15908658 → ACNP
Volume
32
Issue
6
Year of publication
2000
Pages
458 - 467
Database
ISI
SICI code
1590-8658(200008/09)32:6<458:HPCPII>2.0.ZU;2-M
Abstract
Background, in vitro studies showed that Helicobacter pylori strains carryi ng the cag pathogenicity island are able to induce epithelial secretion of Interleukin-8. Aims. To evaluate the assessment of cag pathogenicity island and the expres sion of Interleukin-8 in the gastric mucosa of Helicobao tar pylori-infecte d patients and correlate these data with the activity of gastritis and Heli cobacter pylori density. Methods. cag status was determined by polymerase chain reaction directly on gastric biopsies from 13 Helicobacter pylori+ patients with non-ulcer dysp epsia and 13 Helicobacter pylori+ with duodenal ulcer. Interleukin-8 gene t ranscription and protein expression were analysed by in situ hybridization and immunofluorescence, respectively. Gastritis activity and Helicobacter p ylori density were also investigated. Results. cag was present in 20/26 of Helicobacter pylori+ patients: in 7/13 non-ulcer dyspepsia [53.8%] and in 13/13 duodenal ulcer patients [100%], [ p<0.05]. Interleukin-8 mRNA and protein expression in epithelial and inflam matory cells was higher in cag+ than in cag- patients [p<0.005], Gastritis activity significantly correlated with cag [p<0.05] and Interleukin-8 expre ssion [p<0.005]. Helicobacter pylori density was enhanced in cag+ [p<0.005] and correlated with Interleukin-8 expression [p<0.005]. Conclusions. The present study demonstrates that in Helicobacter pylori-inf ected human gastric mucosa, cag+ infection is associated with enhanced Inte rleukin-8 expression, higher levels of active gastritis and bacterial densi ty, and presence of duodenal ulcer.