Gastric Interleukin‐8 and IgA IL‐8 Autoantibodies in <i>Helicobacter pylori</i> Infection

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.

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“…This work was supported in part by a grant-in-aid for Cancer Research (8)(9)(10)(11)(12)(13)(14) from the Ministry of Health and Welfare, Japan.…”

Section: Acknowledgementsmentioning

confidence: 99%

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

Uemura

Oomoto

Mukai

et al. 1997

Aliment Pharmacol Ther

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“…The cytokine interleukin 8 (IL-8) is a neutrophil chemotactic factor that has been shown to be increased in H. pyloriinfected patients with active gastritis (9). A correlation between type I strains and the ability to induce IL-8 secretion in gastric epithelial cell lines has been demonstrated by several laboratories (10).…”

mentioning

confidence: 99%

Induction of host signal transduction pathways by Helicobacter pylori

Segal

Lange

Covacci

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

187

153

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Adherence of Helicobacter pylori to cultured gastric epithelial cells is associated with several cellular events, including the tyrosine phosphorylation of a 145-kDa host protein; the reorganization of the host cell actin and associated cellular proteins, like vasodilator-stimulated phosphoprotein, adjacent to the attached bacterial cell; and the subsequent release of the cytokine, interleukin 8 (IL-8). H. pylori isolated from patients with ulcer disease and gastric cancer contain a DNA insertion, the cag pathogenicity island (PAI), that is not present in bacteria isolated from individuals with asymptomatic infection. Mutations in a number of PAI genes abolish tyrosine phosphorylation and IL-8 synthesis but not the cytoskeletal rearrangements. Kinase inhibition studies suggest there are two distinct pathways operative in stimulating IL-8 release from host cells and one of these H. pylori pathways is independent of the tyrosine phosphorylation step.

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“…Immune activation following H. pylori infection is manifested by continuous epithelial cell cytokine signaling and gastric mucosal infiltration by neutrophils, macrophages, and lymphocytes. Gastric mucosa of infected patients has increased levels of pro-inflammatory cytokines such as interleukin (IL)-1, tumour necrosis factor alpha, IL-8, and IL-6 [3,4]. IL-1b is a potent proinflammatory cytokine which is involved in the host's response to many antigenic challenges and has biological effects that qualify it as arguably the most important cytokine in the gastrointestinal tract.…”

Section: Introductionmentioning

confidence: 99%

Mucosal IgA & IL-1β in Helicobacter pylori Infection

et al. 2012

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Helicobacter pylori infection stimulates strong local inflammatory and specific IgA antibody production. The influence of antibodies on the bacterial colonization is not clear. Here, we have analysed the association between the mucosal IgA level and IL-1b in various manifestations of the infection seen endoscopically. Antral biopsies of 57 dyspeptic patients were taken for culture, histology and estimation of mucosal levels of anti-H. pylori IgA and IL1b. Mean mucosal IgA level was higher in patients with normal mucosa compared to all other groups and lower IgA level was associated with higher bacterial density. IL-1b was higher in ulcer patients and suspicious malignancy group as compared to normal group and higher level of IL-1b was associated with higher grades of metaplasia. Present study indicates that local immunity seems to have a protective role against H. pylori infection and higher level of IL-1b induced by the pathogen may be associated with metaplasia and carcinogenesis.

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Gastric Interleukin‐8 and IgA IL‐8 Autoantibodies in Helicobacter pylori Infection

Cited by 247 publications

References 44 publications

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

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

Induction of host signal transduction pathways by Helicobacter pylori

Mucosal IgA & IL-1β in Helicobacter pylori Infection

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