Vol. 274, Issue 6, G992-G996, June 1998
H. pylori stimulates gastrin
release from canine antral cells in primary culture
Frank S.
Lehmann1,
Neal
Schiller2,
Timothy
Cover3,
Ritchard
Hatch2,
Rein
Seensalu1,
Kimitoshi
Kato1,
John H.
Walsh1, and
Andrew H.
Soll1
1 CURE: Gastroenteric Biology
Center, University of California, Los Angeles
90073; 2 University of
California, Riverside, California 92521; and3
Division of Infectious Diseases, Vanderbilt
University School of Medicine, Nashville, Tennessee 37232-2605
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.
Helicobacter; extracts; G cells
