Background & aims: Somatostatin regulates gastric function and cell proliferation. We investigated whether exogenous somatostatin modulates Helicobacter pylori proliferation in vitro.
Methods: Bacteria were cultured in 5 mL Brucella broth. Bacterial numbers of H. pylori (ATCC 43504) and Escherichia coli were calculated 48 and 5 hours after incubation, respectively, by counting the colonies on the blood agar. Chemicals were dissolved in absolute methanol and added to the broth at a final methanol concentration of 1%. Intrabacterial guanosine 3',5'-cyclic monophosphate (cGMP) and adenosine 3',5'-cyclic monophosphate (cAMP) levels were measured by radioimmunoassay.
Results: Somatostatin significantly suppressed H. pylori proliferation at levels at or above 10(-11) mol/L. A similar antiproliferative effect was observed with 8-bromo-cGMP. At concentrations at or above 10(-8) mol/L, dibutyryl cAMP slightly but significantly stimulated bacterial proliferation. Gastrin had no effect. Somatostatin antibody immunoglobulin G fraction blocked the antiproliferative effect of somatostatin on ATCC 43504. Scatchard plot showed that ATCC 43504 has one class of binding site with relatively high affinity (Kd, 0.31 nmol/L). Somatostatin at 10(-11) mol/L increased cGMP and cAMP in H. pylori 11-fold and 6-fold, respectively. In contrast, somatostatin neither bound E. coli nor affected its proliferation.
Conclusions: Somatostatin, at a similar level in human gastric juice (approximately 10(-11) mol/L), suppresses H. pylori proliferation mediated in part by a cGMP-dependent pathway in vitro, indicating a possible inhibitory effect of somatostatin in the gastric lumen on H. pylori proliferation in humans.