Study summary · research use only
Zinc: mechanisms of host defense
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses zinc in host defense, drawing on human and cell-culture data. It reports that zinc deficiency in humans decreases serum thymulin activity and shifts T-helper 1 to T-helper 2 function, decreasing IL-2 and reducing natural-killer and T cytolytic cell activity, and may decrease generation of new CD4+ T cells. In cultured HUT-78 cells, zinc deficiency was associated with decreased NF-kappaB activation and Th1 cytokine production; in humans, zinc supplementation was associated with decreased pro-inflammatory cytokine gene expression and oxidative stress markers. In HL-60 cells, zinc deficiency raised TNF-alpha, IL-1beta, and IL-8, while zinc induced the zinc-finger protein A20, which inhibited NF-kappaB. The authors conclude zinc has a role in cell-mediated immunity and acts as an anti-inflammatory and antioxidant agent.
Abstract
Zinc deficiency in humans decreases the activity of serum thymulin (a thymic hormone), which is required for maturation of T-helper cells. T-helper 1 (Th(1)) cytokines are decreased but T-helper 2 (Th(2)) cytokines are not affected by zinc deficiency in humans. This shift of Th(1) to Th(2) function results in cell-mediated immune dysfunction. Because IL-2 production (Th(1) cytokine) is decreased, this leads to decreased activities of natural-killer cell and T cytolytic cells, which are involved in killing viruses, bacteria, and tumor cells. In humans, zinc deficiency may decrease the generation of new CD4+ T cells from the thymus. In cell culture studies (HUT-78, a Th(0) human malignant lymphoblastoid cell line), as a result of zinc deficiency, nuclear factor-kappaB (NF-kappaB) activation, phosphorylation of IkappaB, and binding of NF-kappaB to DNA are decreased and this results in decreased Th(1) cytokine production. In another study, zinc supplementation to humans decreased the gene expression and production of pro-inflammatory cytokines and decreased oxidative stress markers. In HL-60 cells (a human pro-myelocytic leukemia cell line), zinc deficiency increased the levels of TNF-alpha, IL-1beta, and IL-8 cytokines and mRNA. In these cells, zinc induced A20, a zinc finger protein that inhibited NF-kappaB activation via tumor necrosis factor receptor associated factor pathway, and this decreased gene expression of pro-inflammatory cytokines and oxidative stress markers. We conclude that zinc has an important role in cell-mediated immune functions and also functions as antiinflammatory and antioxidant agent.
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