Feeding rodents a diet rich in evening primrose oil (EPO), which contains 5
-10 g gamma-linolenic acid (GLA)/100 g total fatty acids, has been shown to
decrease lymphocyte proliferation and natural killer cell activity. Howeve
r, EPO contains a very high level of linoleic acid which itself can affect
lymphocyte functions and it is not clear to what extent the effects of EPO
can be attributed to GLA. The current study investigated the effect of two
levels of GLA in the rat diet upon immune cell functions; the level of lino
leic acid was maintained below 30 g/100 g total fatty acids. Weanling rats
were fed on high fat (178 g/kg) diets which contained 4.4 g or 10 g GLA/100
g total fatty acids in place of a proportion of linoleic acid. The total p
olyunsaturated fatty acid content and the n-6 to n-3 polyunsaturated fatty
acid ratio of the diet were maintained at 35 g/100 g total fatty acids and
7, respectively. The fatty acid compositions of the serum and of spleen leu
kocytes were markedly influenced by that of the diet, with an increase in t
he proportions of GLA and dihomo-gamma-linolenic acid when the diets contai
ning GLA were fed; these diets also increased the proportion of arachidonic
acid in spleen leukocytes. Spleen lymphocyte proliferation in response to
concanavalin A was significantly reduced (by 60%) by feeding the diet conta
ining the higher level of GLA, but not by the diet containing the lower lev
el of GLA. Spleen natural killer cell activity and prostaglandin E (PGE) pr
oduction by spleen leukocytes were not significantly affected by inclusion
of GLA in the diet, although there was a tendency towards decreased natural
killer cell activity by cells from rats fed the high GLA diet. Thus, this
study shows that dietary GLA is capable of altering the fatty acid composit
ion of cells of the immune system and of exerting some immunomodulatory eff
ects, but that the level of GLA in the diet must exceed 4.4 g/100 g total f
atty acids for these effects to become apparent.