Mucosal interleukin-8 and Helicobacter pylori-associated gastroduodenal disease

Abstract

Objective: To review the role of interleukin (IL)-8 in the immunopathology of Helicobacter pylori-associated gastroduodenal disease.

Method: Literature review.

Results: In H. pylori infection, IL-8 secretion by the gastric mucosa is increased, particularly in patients with active neutrophilic gastritis. Immunoreactive IL-8 is evident in the epithelium of histologically normal gastric mucosa but epithelial IL-8 expression is increased in H. pylori-associated chronic gastritis. Gastric epithelial cell lines constitutively express IL-8 messenger (m)RNA and IL-8 message and protein secretion can be upregulated by the cytokines tumour necrosis factor-alpha, IL-1 alpha and IL-1 beta. H. pylori also directly induces epithelial IL-8 expression in a strain-specific manner. Cytotoxic strains expressing the CagA protein upregulate IL-8 mRNA and IL-8 protein secretion.

Conclusion: IL-8 is an important chemotactic and activating factor for neutrophils. The secretion of IL-8 by epithelial cells is probably a key factor in host defences at mucosal sites, permitting a rapid polymorph response against infectious agents. If defence mechanisms fail and chronic infection results, continued upregulation of IL-8 and neutrophil activation could lead to mucosal damage and increased free radical formation. Mucosal IL-8 production in H. pylori infection may be an important factor in the immunopathogenesis of peptic ulcer disease and also be of relevance to gastric carcinogenesis.