Gastric corpus IL‐8 concentration and neutrophil infiltration in duodenal ulcer patients
Open Access
- 1 July 1997
- journal article
- clinical trial
- Published by Wiley in Alimentary Pharmacology & Therapeutics
- Vol. 11 (4) , 793-800
- https://doi.org/10.1046/j.1365-2036.1997.00218.x
Abstract
Background: The purpose of the present study was to examine the association between interleukin‐8 (IL‐8) in the gastric body due to Helicobacter pylori infection and histological gastritis, as well as elucidating the effect of acid secretion inhibitors on H. pylori associated body gastritis in duodenal ulcer patients. Methods: Twenty H. pylori‐negative patients, 20 H. pylori‐positive patients with chronic gastritis without peptic ulceration, and 20 H. pylori‐positive duodenal ulcer patients (DU) were studied. Four biopsy samples were taken, each from the greater curvature of the antrum and body of the stomach. Biopsies were histologically investigated by ELISA to determine the density of H. pylori, the degree of neutrophil infiltration and the IL‐8 concentration in the mucosa. Results: In the gastric mucosa of H. pylori‐negative subjects, no IL‐8 and hardly any neutrophil infiltration were observed. In contrast, enhanced IL‐8 production and increased neutrophil infiltration were present in those infected with H. pylori. In H. pylori‐positive patients, a significant correlation was observed between the IL‐8 concentration and the degree of neutrophil infiltration, but no correlation was found in the body mucosa of those with DU. Twelve of 20 DU patients demonstrated hardly any neutrophil infiltration, despite the increased mucosal IL‐8 content in the body. The administration of omeprazole in DU patients markedly increased mucosal neutrophil infiltration even though it did not cause any significant change in the H. pylori density and IL‐8 concentration in the body. Although the effect of omeprazole was transient, a significant increase in neutrophil infiltration continued in comparison with the status before omeprazole administration in those subsequently undergoing maintenance treatment with H2‐blockers. Conclusion: In H. pylori‐positive chronic gastritis, IL‐8 concentration is enhanced in the mucosa of the body, and is associated with increased neutrophil infiltration. However, in DU patients, despite increases in body IL‐8 concentration, neutrophil infiltration is reduced and the gastritis may be localized in the antrum.Keywords
This publication has 17 references indexed in Scilit:
- Classification and Grading of GastritisThe American Journal of Surgical Pathology, 1996
- Atrophic Gastritis andHelicobacter pyloriInfection in Patients with Reflux Esophagitis Treated with Omeprazole or FundoplicationNew England Journal of Medicine, 1996
- Helicobacter pylori induced interleukin-8 expression in gastric epithelial cells is associated with CagA positive phenotype.Journal of Clinical Pathology, 1995
- Distribution of Helicobacter pylori colonisation and associated gastric inflammatory changes: difference between patients with duodenal and gastric ulcers.Journal of Clinical Pathology, 1993
- Gastric Interleukin‐8 and IgA IL‐8 Autoantibodies in Helicobacter pylori InfectionScandinavian Journal of Immunology, 1993
- Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammationGastroenterology, 1992
- Helicobacter pyloriInfection and Gastric Carcinoma among Japanese Americans in HawaiiNew England Journal of Medicine, 1991
- Helicobacter pyloriInfection and the Risk of Gastric CarcinomaNew England Journal of Medicine, 1991
- Association between infection with Helicobacter pylori and risk of gastric cancer: evidence from a prospective investigation.BMJ, 1991
- The Sydney System: Epidemiology and natural history of chronic gastritisJournal of Gastroenterology and Hepatology, 1991