# VITAMIN E AND THE AGING IMMUNE RESPONSE

> **NIH NIH R01** · TUFTS UNIVERSITY BOSTON · 1991 · $108,050

## Abstract

Aging is associated with a decline in immunological vigor which can
contribute to development of age-associated diseases.  Nutritional
manipulation of the aged immune system presents a practical approach to
improving immune response.  However, in depth studies of nutrition and the
immune system especially as they relate to aging, are lacking.  We have
shown that macrophages (Mo) from aged mice and humans synthesize more PGE2
(shown to have suppressing effect on cell-mediated immunity) than young
mice and humans.  Furthermore, vitamin E supplementation decreases PGE2
production and enhances IL-2 production an lymphocyte mitogenesis in aged
mice and humans.  It is proposed that increases in Mo-mediated suppression
via cyclooxygenase and lipoxygenase metabolites of arachidonic acid (AA),
i.e., PGE2, leukotriene (LT), hydroxyeicosatetranoic acid (HETE) of H2O2
formation, contributes to the age-associated decrease in IL-2 production
and lymphocyte proliferation.  Furthermore, vitamin E supplementation,
through antioxidant dampening of cyclooxygenase or lipoxygenase or
terminating propagation of lipid peroxidation will decrease this
suppression, thereby increasing IL-2 production and lymphocyte mitogenesis.

To test this hypothesis we will:  1) compare Mo production of AA
metabolites, H2O2 and IL-2 and IL-1 production by mixtures of splenic Mo
and T cells from young and old mice fed semi-purified diets with 30 or 500
ppm vitamin E.  The contribution of each metabolite will be further
assessed by addition of its inhibitor or the metabolite itself to these
cultures.  The effect of in vitro addition of vitamin E will be compared to
that of cyclooxygenase and lipoxygenase inhibitors, catalase and
supplementation of vitamin E with different levels of tocopherol (30, 60,
120, 240, 500 ppm) on the immune response of mice will be studied.  Through
these studies:  1) the contribution of oxidative Mo metabolites to age-
associated changes in immune function will be studied; 2) the mechanism of
the immunostimulatory effect of vitamin E in mice will be delineated; and
3) an appropriate dietary level of tocopherol for optimal immune
responsiveness in aged mice and the continuation of the effect over long
periods of time will be determined.

## Key facts

- **NIH application ID:** 3120917
- **Project number:** 5R01AG009140-02
- **Recipient organization:** TUFTS UNIVERSITY BOSTON
- **SAM.gov UEI:** C1F5LNUF7W86
- **Principal Investigator:** SIMIN Nikbin MEYDANI
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1991
- **Award amount:** $108,050
- **Award type:** 5
- **Project period:** 1990-05-01 → 1993-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3120917

## Citation

> US National Institutes of Health, RePORTER application 3120917, VITAMIN E AND THE AGING IMMUNE RESPONSE (5R01AG009140-02). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3120917. Licensed CC0.

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