Zinc Supplementation in the Elderly Reduces Spontaneous Inflammatory Cytokine Release and Restores T Cell Functions

Rejuvenation Res. 2008 Feb;11(1):227-37. doi: 10.1089/rej.2007.0613.

Abstract

Aging is associated with low-grade inflammation on the one hand and mild zinc deficiency on the other. These conditions contribute to decreased immune functions, resulting in increased incidences of infections and autoimmune diseases. The aim of this study was to give more insight into the question, to what extent is low-grade inflammation caused by zinc deficient status. Here we report the effect of improved intracellular zinc status on low-grade inflammatory activity in 19 healthy elderly subjects. Our experiments show that adjustment of labile zinc by moderate zinc supplementation reduces spontaneous cytokine release and defects in termination of inflammatory activity. This results in reduced amounts of unspecific preactivated T cells and leads to improved T cell response upon mitogenic stimulation. Therefore, in contrast to other anti-inflammatory drugs, zinc does not suppress, but improves immune reaction upon pathogen invasion. These results suggest that mildly zinc-deficient, healthy elderly subjects might benefit from moderate zinc supplementation due to a more balanced immune response with reduced incidences of infections and autoimmune diseases.

Publication types

  • Comparative Study
  • Evaluation Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged*
  • Aged, 80 and over
  • Cation Transport Proteins / genetics
  • Cells, Cultured
  • Cytokines / metabolism
  • Dietary Supplements*
  • Down-Regulation / drug effects
  • Female
  • Gene Expression Regulation / drug effects
  • Humans
  • Inflammation Mediators / metabolism*
  • Intestinal Absorption / genetics
  • Leukocytes / drug effects
  • Leukocytes / metabolism
  • Lipopolysaccharides / pharmacology
  • Male
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / physiology
  • Zinc / metabolism
  • Zinc / pharmacology*

Substances

  • Cation Transport Proteins
  • Cytokines
  • Inflammation Mediators
  • Lipopolysaccharides
  • SLC39A1 protein, human
  • SLC39A2 protein, human
  • SLC39A3 protein, human
  • Zinc