Helicobacter pylori lipopolysaccharide inhibition of gastric mucosal somatostatin receptor.
A gastric mucosal somatostatin receptor was isolated from the solubilized epithelial cell membrane by affinity chromatography on a column consisting of covalently coupled [D-Tryp8]SRIF-14 to Affi-Gel 10. The receptor protein displayed a molecular weight of 61kDa and exhibited specific affinity towards 125I-labeled [Tyr11]SRIF-14 with the optimum range of 4-8 micrograms/ml. The binding of somatostatin to its mucosal receptor was inhibited by lipopolysaccharide from H. pylori. The inhibitory effect was proportional to the concentration of lipopolysaccharide up to 50 micrograms/ml and reached a maximum of 94.1% inhibition. The results suggest that H. pylori, through its lipopolysaccharide, is capable of interfering with somatostatin regulatory effect on gastric mucosal G-cell function.
Piotrowski
J
J
Research Center, University of Medicine and Dentistry of New Jersey, Newark 07103-2400, USA.
Majka
J
J
Slomiany
A
A
Slomiany
B L
BL
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism*; D016998:Helicobacter / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism / Q000494:pharmacology*; D011869:Radioligand Assay; D051381:Rats; D017481:Receptors, Somatostatin / Q000037:antagonists & inhibitors*
D008070:Lipopolysaccharides; D017481:Receptors, Somatostatin