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Nutrition and Age-Associated Inflammation: Implications for Disease PreventionFrom the JMUSDA Human Nutrition Research Center on Aging at Tufts University and Friedman School of Nutrition Science and Policy, Tufts University, Boston, Massachusetts. Address correspondence to: Simin Nikbin Meydani, Nutritional Immunology Laboratory, JMUSDA-HNRCA at Tufts University, 711 Washington Street, Boston, MA 02111; e-mail: simin.meydani{at}tufts.edu.
Accumulating evidence suggests that aging is associated with dysregulated
immune and inflammatory responses. Investigation into the cellular and
molecular mechanisms underlying this phenomenon suggests that an up-regulated
cyclooxygenase (COX)-2 expression, and resulting increase in production of
prostaglandin E2 (PGE2), is a critical factor.
Macrophages from old mice have significantly higher levels of PGE2
production compared with those from young mice, a result of increased COX-2
expression and protein levels leading to increased COX enzyme activity.
Furthermore, studies suggest that the age-associated increase in macrophage
PGE2 production is due to ceramide-induced up-regulation of nuclear
factor-
Key Words: aging inflammatory response macrophages (M
Journal of Parenteral and Enteral Nutrition, Vol. 32, No. 6,
626-629 (2008) |
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B activation. Such processes may also occur in cell types other
than macrophages, lending further insight into potential mechanisms of
age-related diseases. Moreover, the excess PGE2 induces harmful
effects in other cell types such as T cells and adipocytes through the
negative crosstalk between macrophages with other cells, resulting in further
increased susceptibility to diseases. Nutrient/dietary medications, such as
antioxidants and certain lipids have suggested a promising route to reduce the
age-related increase in COX activity and PGE2 production that is
associated with several disease states.
) ceramide sphingomyelinase cyclooxygenase (COX)-2 prostaglandin E2 (PGE2) nuclear factor-kappa B (NF