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Scand J Immunol. 1993 Jan;37(1):65-70.

Gastric interleukin-8 and IgA IL-8 autoantibodies in Helicobacter pylori infection.

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1
Department of Clinical Medicine, St James's University Hospital, Leeds, UK.

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.

[Indexed for MEDLINE]

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