Mononuclear cells and cytokines stimulate gastrin release from
canine antral cells in primary culture.
Lehmann, Frank S., Ellen H. Golodner, Jianyi Wang, Monica C. Y. Chen,
Debbie Avedian, John Calam, John H. Walsh, Steven Dubinett, and
Andrew H. Soll.
CURE/UCLA Gastroenteric Biology Center and Pulmonary Immunology
Labaratory, VA Wadsworth Medical and Research Services and Department
of Medicine, University of California Los Angeles, Los Angeles,
California 90073
APStracts 3:0041G, 1996.
Patients with H.pylori-associated gastritis have an increased release
of gastrin. The mechanisms by which H.pylori affects the endocrine
cells are unclear. We have used primary cultures containing canine
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
-dependently. Separating mononuclear cells from G-cells by Transwell
filters with 0.4 [mu]m pore size still produced a significant
increase of gastrin release. Three human recombinant cytokines,
interferon-g, tumour necrosis factor-[alpha] and interleukin-2, but
not interleukin-6 and interleukin-1b, produced each dose-dependent
increases of gastrin stimulation. NH4Cl did not stimulate gastrin
release. We conclude that mononuclear cells and purified monocytes
prepared from human blood, as well as several cytokines, stimulate
gastrin release from antral G-cells. These factors may play an
important role in the pathogenesis of H.pylori-associated
hypergastrinaemia.
Received 1 August 1994; accepted in final form 27 November 1995.
APS Manuscript Number G285-4.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 14 February 96