Modulation of age-related alterations in membrane composition and receptor-associated immune functions by food restriction in Fischer 344 rats.
Food restriction is known to modulate aging and age-associated immune functions in rodents. In an attempt to understand the mechanism(s) through which food restriction delays age-associated loss of certain immune functions, lipid composition of spleen cells as well as binding of spleen cells to interleukin-2 (IL-2) and insulin were analyzed in four month-old and 19-month-old ad libitum fed (AL) and food-restricted (FR) Fischer-344 male rats. The results revealed that although AL-fed rats did not show a difference in age-related changes for IL-2 and insulin binding, the number of binding sites were significantly increased in the spleen cells of 19-month-old FR animals when compared with those of the 19-month-old AL group. When spleen cell phospholipid fractions were analyzed for fatty acid composition, the spleen cells from FR animals consistently revealed higher linoleic acid (18:2) levels and significantly lower arachidonic acid (20:4) and long chain fatty acid, docosatetraenoic acid (22:4) levels in the phosphatidylcholine and phosphatidylethanolamine fractions than the spleen cells of the AL rats. Further, spleen cell plasma membranes of FR rats also exhibited similar changes showing higher 18:2 and lower 20:4 and 22:4 levels than the AL animals. Finally, spleen cells obtained from 19-month-old FR animals produced higher levels of IL-2 and lesser prostaglandin E2 when compared to 19-month-old AL animals. The above observations suggest that one of the mechanisms through which food restriction may delay the loss of age-associated immune functions is through modulation of the fatty acyl composition of phospholipid fractions of spleen cell membranes. This modification may facilitate binding of IL-2 and insulin to their receptors and thus may improve T cell proliferation and prevent or delay age-related loss in immune functions.
Venkatraman
J
J
Department of Medicine, University of Texas Health Science Center, San Antonio 78284-7874.
Fernandes
G
G
D000375:Aging / Q000276:immunology* / Q000378:metabolism; D000818:Animals; D002462:Cell Membrane / Q000276:immunology / Q000378:metabolism; D015232:Dinoprostone / Q000096:biosynthesis; D005227:Fatty Acids / Q000378:metabolism; D005508:Food Deprivation / Q000502:physiology*; D007328:Insulin / Q000378:metabolism; D007376:Interleukin-2 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D008297:Male; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D013154:Spleen / Q000276:immunology / Q000378:metabolism
D005227:Fatty Acids; D007328:Insulin; D007376:Interleukin-2; D010743:Phospholipids; D015375:Receptors, Interleukin-2; D015232:Dinoprostone