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Immune Response of Elderly Could Get Shot in ArmBy Judy McBride
January 12, 1998
Imagine having an immune system that's as vigilant against infections and would-be tumors at age 70 as it was at age 20. Or one that won't turn on you later in life, causing the aches and pains of rheumatoid arthritis or other inflammatory diseases.
That dream is a little closer to reality at the USDA Human Nutrition Research Center on Aging at Tufts University, Boston. The center is funded by USDA's Agricultural Research Service.
Scientists there have identified the instigator behind the age-related decline in T cell function--which coordinates the body's response to an infectious agent. What's more, they were able to reduce the effects of this instigator in cultured cells.
Nutritional immunologist Simin Nikbin Meydani and her colleagues suspected that prostaglandin E2 (PGE2) might contribute to the decline of T cell function in seniors because too much of this inflammation-producing substance has been shown to suppress T cell activity.
Suspicions were confirmed when the scientists compared white blood cells from old and young mice. Macrophages from the old mice indeed produced more PGE2, which reduced T cell function. While it's not the only culprit, it appears to be an important one, the researchers say. They speculate that excess PGE2 may also contribute to cancer, cardiovascular disease, arthritis and other diseases of aging because the fatty substance is found in new tumors as well as in inflamed tissues, including artery walls.
The researchers also demonstrated that excess PGE2 was due to increased levels and activity of the enzyme cyclooxygenase, needed to produce PGE2.
Adding the antioxidant vitamin E to the cell cultures reduced PGE2 levels and improved T cell function. This suggests that people might slow dysfunction of the immune system as they age by increasing body levels of vitamin E and possibly other nutrients.
Scientific contact: Simin Nikbin Meydani, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, phone (617) 556-3129, fax (617) 556-3224, email@example.com.