MONONUCLEAR-CELLS AND CYTOKINES STIMULATE GASTRIN-RELEASE FROM CANINEANTRAL CELLS IN PRIMARY CULTURE

Patients with Helicobacter pylori-associated gastritis have an increas ed release of gastrin. The mechanisms by which H. pylori affects the e ndocrine cells are unclear. We have used primary cultures containing c anine antral G cells to examine the effects of human blood mononuclear cells, purified monocytes and lymphocytes, recombinant cytokines, and NH4Cl on gastrin release. Mononuclear cells and purified monocytes in direct contact with G cells stimulated gastrin release dose dependent ly. Separating mononuclear cells from G cells by Transwell filters wit h 0.4-mu m pore size still produced a significant increase of gastrin release. Three human recombinant cytokines, interferon-gamma, tumor ne crosis factor-alpha, and interleukin-2, but not interleukin-6 and inte rleukin-1 beta, each produced dose-dependent increases of gastrin stim ulation. NH4Cl did not stimulate gastrin release. We conclude that mon onuclear cells and purified monocytes prepared from human blood, as we ll as several cytokines, stimulate gastrin release from antral G cells . These factors may play an important role in the pathogenesis of H. p ylori-associated hypergastrinemia.