H. pylori stimulates gastrin release from canine antral cells in primary culture
Lehmann, F.S.; Schiller, N.; Cover, T.; Hatch, R.; Seensalu, R.; Kato, K.; Walsh, J.H.; Soll, A.H.
American Journal of Physiology 274(6): G992-G996
1998
ISSN/ISBN: 0002-9513 PMID: 9696722 Document Number: 494823
Patients chronically infected with Helicobacter pylori are known to have hypergastrinemia. Previous studies have demonstrated the stimulation of gastrin from isolated G cells by monocytes and cytokines. The aim of this study was to determine if H. pylori can directly stimulate gastrin secretion. The secretion of gastrin from canine G cells in 48-h primary cultures was investigated using either live H. pylori bacteria or various bacterial extracts from three well-characterized strains. Whole bacterial sonic extracts and water-extracted surface proteins, but not PBS extracts, from strains 43579 (CagA+/VacA+), 60190 (CagA+/VacA+), and 60190:v1 (CagA+/VacA-) significantly stimulated gastrin release. Controls demonstrated that gastrin stimulation by the sonic extracts was not due to a direct toxic effect on G cells. We conclude that H. pylori produces a soluble factor(s), which can directly stimulate gastrin release in enriched canine G cell cultures. This stimulatory effect may play an important role in the H. pylori-associated hypergastrinemia and subsequent development of peptic ulcer disease. Reprinted by permission of the publisher.