Gastric corpus IL‐8 concentration and neutrophil infiltration in duodenal ulcer patients

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.

Bacterial Load and Degree of Gastric Mucosal Inflammation in <i>Helicobacter pylori</i> Infection

“…Interestingly, they reported that in the corpus of CagA+ gastritis cases, H. pylori density was significantly higher than in DU cases (5.7 vs. 4.3 × 10 5 CFU/mg protein, p < 0.05), but did not correlate with either PNC or mononuclear cell infiltration (MNC) in both gastritis and DU. Inadequate cellular inflammatory response in the corpus in cases of antral predominant gastritis have been commonly observed and explained by host factors, especially high acid secretion [10]. On the other hand, in both the antrum and corpus, the relation between the number of CFU and IL-1β and IL-8 expression describes a dose-response curve [IL-1β: PNC and MNC each p < 0.0001 (antrum) and p < 0.0005 (corpus); IL-8: PNC and MNC each p < 0.0001 for antrum and corpus].…”

The role of CXC chemokines in the transition of chronic inflammation to esophageal and gastric cancer

“…Moreover, the expression of GRO-α in patients with H. pylori-negative chronic gastritis was significantly higher than in patients with normal gastric mucosa [52]. Additionally, IL-8 and GRO-α have been demonstrated to be higher in patients (suffering from gastritis) with duodenal or peptic ulcers than in patients without these complications [50,[56][57][58][59]. Furthermore, expression of GRO-α and ENA-78 was significantly increased in H. pylori-infected mucosa of smokers compared with non-smokers [60].…”

Downregulation of immunomodulator gene expression in LPS-stimulated human polymorphonuclear leukocytes by the proton pump inhibitor lansoprazole

“…4 In particular, IL-8 is thought to be important in initiating and perpetuating the infl ammatory process, 1-3,6,21 and mucosal IL-8 correlates with the infi ltration of PMNs in H. pylori-associated gastritis. 7 In 1999, Capodicasa et al 22 reported that LPZ at 100 μM (36.9 μg/ml) to 1000 μM (369 μg/ml) induced signifi cant dose-dependent inhibition of chemotaxis and ROS generation exerted by PMNs. In the present study, we analyzed the mRNA levels of fi ve types of immunomodulator genes in PMNs activated by LPS, and all of them were downregulated after 3-h treatment with LPZ at ≥0.01 μg/ml, in a dose-dependent manner.…”

“…5,6 Prolonged secretion of IL-8 by gastric epithelial cells may result in the recruitment of PMNs to gastric tissues. 7 Infi ltrated PMNs may release a number of proinfl ammatory cytokines, reactive oxygen species (ROS), and chemical mediators, which further contribute to the progression of the infl ammatory process.…”