Abstract
An individual's zinc status has a significant impact on the immune system, and zinc deficiency, as well as supplementation, modulates immune function. To investigate the effects of zinc on different leukocyte subsets, we used microarray technology to analyze and compare the changes in mRNA expression in cell culture models of monocytes (THP-1), T cells (Jurkat), and B cells (Raji), in response to supplementation for 40 h with 50 microM zinc or 2.5 microM of the membrane-permeant zinc chelator TPEN [N,N,N',N'-tetrakis-(2-pyridyl-methyl)ethylenediamine], respectively. In each cell type, several hundred genes were identified to be zinc sensitive, but only a total of seven genes were commonly regulated in all three cell lines. The majority of those genes were involved in zinc homeostasis, and none in immune function. Nevertheless, further analysis revealed that zinc affects entire functional networks of genes that are related to proinflammatory cytokines and cellular survival. Although the zinc-regulated activities are similar throughout the gene networks, the specific genes that are affected vary significantly between different cell types, a situation that helps to elucidate the disparity of the effects that zinc has on different leukocyte populations.
Highlights
Zinc ions were found to affect multiple cellular signaling pathways on the molecular level [1], suggesting zinc may play a role in the regulation of a considerable number of genes
Three human leukocyte cell lines, THP-1, Jurkat (T cells), and Raji (B cells), were cultured in the presence of 50 μM ZnSO4 or 2.5 μM of the membrane permeant zinc chelator TPEN for 40 h to compare the effect of zinc supplementation or deprivation on different types of leukocytes
In the leukocyte models investigated here, the functional networks contained genes that were mainly involved in inflammation and cellular survival
Summary
Zinc ions were found to affect multiple cellular signaling pathways on the molecular level [1], suggesting zinc may play a role in the regulation of a considerable number of genes. This zinc function has been confirmed by microarray experiments investigating the effects of zinc supplementation and/or deprivation. In elderly people, who have a high risk of zinc deficiency, zinc supplementation improves responsiveness to immunization, serum thymulin activity, delayed type hypersensitivity reactions, and T-cell proliferation in response to mitogens [11]
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