Abstract
Little is known about whether Helicobacter pylori infection alters fatty acid metabolism in gastric mucosal cells. By using cultured rat gastric mucosal cells (RGM-1), we investigated the effect of H. pylori broth culture filtrates on this point. Furthermore, our study aimed to find out whether n-6 long chain polyunsaturated fatty acids from linoleic acid are formed in RGM-1 cells. Rat gastric mucosal cells were incubated with 10, 20 and 40 microg/mL of linoleic acid or medium alone. Phosphatidylcholine content extracted from whole RGM-1 cells was quantitated by using a densitometer, and its fatty acid composition was analyzed by using gas chromatography. Prostaglandin E2 concentration in the culture medium was measured by using radioimmunoassay. The expression of cyclooxygenase (COX)-1 and COX-2 was examined by using reverse transcription-polymerase chain reaction. In addition, after incubation with [1-14C] linoleic acid, radioactivities of both linoleic acid and arachidonic acid components of the PC fraction were counted. The effects of H. pylori broth culture filtrates on PC content, its fatty acid composition and prostaglandin (PG)E2 synthesis were also assessed. Linoleic acid addition caused an increase in the composition of arachidonic acid, as well as linoleic acid, and also in PGE2 concentration. Cyclo-oxygenase-2 expression was induced in RGM-1 cells by the addition of linoleic acid. In addition, [1-14C] linoleic acid added to the culture medium was converted to [1-14C] arachidonic acid in RGM-1 cells. Helicobacter pylori broth culture filtrates decreased linoleic acid composition and increased arachidonic acid composition. Moreover, after incubation with H. pylori broth culture filtrates, PGE2 concentrations were higher than that of the controls. These findings suggest the presence of fatty acid elongase and Delta5- and Delta6-desaturases synthesize arachidonic acid from linoleic acid in RGM-1 cells. Thus, H. pylori infection may enhance PGE2 synthesis and accelerate n-6 fatty acid metabolism in gastric mucosal cells, which could make the gastric mucosal barrier more fragile.
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