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

Abstract

Gastric infection with Helicobacter pylori is frequently characterized by neutrophil infiltration. The production of the neutrophil‐activating peptide (NAP‐1/IL‐8) and mucosal IgA autoantibodies to IL‐8 by human antral biopsies have been examined during short‐term in vitro culture. Detectable IL‐8 was secreted by 84% of H. pylori‐negative patients with normal antral mucosa (range <0.07–61.5 ng/mg biopsy protein, n=19). Concentrations in 4 patients with reactive gastritis and 10 with inactive gastritis were not significantly different from subjects with normal mucosa. In H. pylori‐positive patients with active gastritis and neutrophil infiltration into the epithelium (n=17) IL‐8 secretion was significantly increased relative to subjects with normal mucosa (p > 0.0001), inactive gastritis (p <0.001) and reactive gastritis (P<0.01). IL‐8 concentrations in active gastritis were significantly correlated with the extent of epithelial surface degeneration (r=0.64). IgA autoantibodies were present in 19 patients (13 active, 4 inactive gastritis) and concentrations were significantly correlated with IL‐8 production (p<0.001). Gastric synthesis of IL‐8 is likely to be an important factor in regulating mucosal neutrophil infiltration and activation in patients with H. pylori infection. The local production of IgA antibodies to IL‐8 may represent a down‐regulatory response of the host to limit mucosal damage associated with a chronic bacterial infection.