Correlation of kinin generating activity with Helicobacter pylori-associated gastric infection

The kallikrein-kinin system involves a biologically complex set of interactive proteases that signal the first-line onset of inflammation and associated cellular processes. The basic enzymatic cleavage of kininogen substrate by the serine protease tissue kallikrein to liberate kinins is regulated by a number of factors. These may include the recently discovered bacterial involvement in the causation of gastritis. The gram-negative Helicobacter pylori organism, colonises the human gastric epithelium and initiates ulcerogenesis and may induce, in the longer term, tumour formation. The aim of this study was to investigate the role of kinins in H. pylori-induced gastric dyspepsia. During endoscopic examination, lavage aspirates of 23 patients were collected, and the tissue kallikrein content measured by a kinin-generating assay and an enzyme-linked immunosorbent assay. Gastric antral and pyloric biopsy tissue was histologically examined for degrees of inflammation and H. pylori infection, and then immunolabelled for tissue kallikrein and kinin receptors. Results show that labelled tissue kallikrein in the fundic glands and parietal cells of the diseased antrum was elevated with increasing severity of gastritis. Further, kinin-generating potential of the lavage fluid appeared to be greater with increasing evidence of infection. Tissue kallikrein immunosorbent assay levels were significantly raised in patients showing mild to moderate H. pylori infection. One outcome of this study may be the inclusion of kinin antagonists in management of gastric dyspepsia.