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Inhibition of human gastric cyclic AMP production by Helicobacter pylori protein—possible involvement of mucosal prostaglandin E 2
Author(s) -
TAHA A. S.,
FRASER W. D.,
KELLY R. W.,
GEMMELL C. G.,
LEE F. D.,
RUSSELL R. I.
Publication year - 1991
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.1991.tb00041.x
Subject(s) - histamine , helicobacter pylori , prostaglandin e , prostaglandin , medicine , gastric mucosa , endocrinology , prostaglandin e2 , second messenger system , stomach , receptor
SUMMARY The effect of Helicobacter pylori protein on cAMP and prostaglandin (PGE 2 ) production was studied in incubates of human gastric fundic mucosa. At 24 hours, specimens incubated in the control fluid had a median cAMP value of 81 pmol/mg protein, compared to 28 pmol/mg ( P < 0.05) when incubated in H. pylori protein, 155 pmol/kg ( P < 0.006) in histamine, and 23 pmol/kg ( P < 0.05) in histamine plus H. pylori protein. A similar trend was observed at 48 hours. Although H. pylori protein had no direct effect on mucosal PGE 2 , it intensified the inhibitory effect of indomethacin and prevented the stimulatory effect of histamine on both PGE 2 and cAMP production. Given the role of cAMP in various physiological responses, these results suggest that H. pylori protein might alter those functional aspects of the human gastric mucosa which rely on cAMP as a second messenger. Assuming that PGE 2 is involved in mediating such effect, its role would appear to be either partial or indirect.