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Macrophage prostaglandin production contributes to the age-associated decrease in T cell function which is reversed

A A Beharka1, D Wu, S N Han

  • 1Nutritional Immunology Laboratory, Jean Mayer Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA.

Mechanisms of Ageing and Development
|February 1, 1997
PubMed
Summary

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Aging impairs T cell immunity, partly due to increased prostaglandin E2 (PGE2) from macrophages. Antioxidants like vitamin E reduce PGE2, enhancing T cell function in older mice.

Area of Science:

  • Immunology
  • Aging Research
  • Cellular Biology

Background:

  • Aging is linked to reduced T cell immunity, evidenced by lower interleukin-2 (IL-2) production and proliferation.
  • Macrophages (M phi) from aged mice produce more prostaglandin E2 (PGE2), a known suppressor of T cell functions.

Purpose of the Study:

  • To investigate the hypothesis that elevated PGE2 contributes to age-related T cell dysfunction.
  • To determine if reducing PGE2 production with dietary antioxidants can restore T cell function in aging.

Main Methods:

  • Co-culturing purified T cells and macrophages (M phi) from young and old C57BL/6N1A mice.
  • Assessing T cell proliferation and IL-2 secretion in response to Concanavalin A (ConA).
  • Evaluating the effects of adding PGE2, hydrogen peroxide (H2O2), catalase, indomethacin, and vitamin E on T cell cultures.

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Main Results:

  • Co-cultures with M phi from old mice showed reduced T cell proliferation and IL-2 secretion compared to young mice.
  • Exogenous PGE2 suppressed T cell responses in young but not old mice.
  • Indomethacin and vitamin E, which reduced PGE2 production, significantly improved T cell proliferation and IL-2 secretion.

Conclusions:

  • Increased PGE2 production by macrophages is a key factor in age-associated decline of T cell-mediated immunity.
  • Vitamin E enhances T cell responsiveness in aged mice primarily by decreasing M phi PGE2 production, with a potential direct effect on T cells also noted.