QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Prasad, A. S. Search for Related Content PubMed PubMed Citation Articles by Prasad, A. S.

---

Symposium: Micronutrient Regulation of Host-Pathogen Interactions

Zinc: Mechanisms of Host Defense^1–3,

Department of Internal Medicine, Division of Hematology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan 48201

^* To whom correspondence should be addressed. E-mail: prasada{at}karmanos.org.

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 (Th₁) cytokines are decreased but T-helper 2 (Th₂) cytokines are not affected by zinc deficiency in humans. This shift of Th₁ to Th₂ function results in cell-mediated immune dysfunction. Because IL-2 production (Th₁ 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 Th₀ human malignant lymphoblastoid cell line), as a result of zinc deficiency, nuclear factor-B (NF-B) activation, phosphorylation of IB, and binding of NF-B to DNA are decreased and this results in decreased Th₁ 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-, IL-1ß, and IL-8 cytokines and mRNA. In these cells, zinc induced A20, a zinc finger protein that inhibited NF-B 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.

This article has been cited by other articles:

				M. C. Cave, R. T. Hurt, T. H. Frazier, P. J. Matheson, R. N. Garrison, C. J. McClain, and S. A. McClave Obesity, Inflammation, and the Potential Application of Pharmaconutrition Nutr Clin Pract, February 1, 2008; 23(1): 16 - 34. [Abstract] [Full Text] [PDF]

				A. M. Prentice, H. Ghattas, and S. E. Cox Host-Pathogen Interactions: Can Micronutrients Tip the Balance? J. Nutr., May 1, 2007; 137(5): 1334 - 1337. [Abstract] [Full Text] [PDF]