The Effect of Intracellular Zinc Concentration on Immune Activation and Proinflammatory Response in THP-1 Monocytes Public Deposited

http://ir.library.oregonstate.edu/concern/undergraduate_thesis_or_projects/c821gm58t

Presentation entitled: The Effect of Intracellular Zinc Concentration on Immune Activation and Proinflammatory Response in THP-1 Monocytes/ by Nicole Rinaldi, Carmen Wong and Emily Ho

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  • Zinc is an essential micronutrient required for many cellular functions, including the development and function of the immune system. The biological consequences of zinc deficiency illustrate the significance of zinc in human health. Zinc deficiency has been shown to cause the dysregulation of both innate and adaptive immune responses, as well as promote the development of chronic low-grade inflammation. Interestingly, the effects of aging and zinc deficiency on the immune system are remarkably alike, as aging is also strongly associated with impaired immune function and chronic low-grade inflammation. In fact, the older population is particularly susceptible to zinc deficiency, and zinc status declines with age. It is therefore thought that age-related zinc deficiency may contribute to the chronic inflammation commonly observed in the elderly. In contrast to severe zinc deficiency, the effect of marginal zinc deficiency on chronic inflammation is not well characterized. Additionally, the effect of zinc supplementation on immune function is unclear, since clinical trials of zinc supplementation exhibit conflicting results. The central questions of this study are whether marginal zinc deficiency contributes to immune dysregulation, resulting in an enhancement of immune cell activation and increased inflammatory response, and whether zinc supplementation can reduce immune activation and decrease inflammation. Using cultured THP-1 human leukemic monocytic cells, we studied the impact of marginal zinc deficiency and zinc supplementation on the expression of well-known mediators of immune activation and proinflammatory response. We found zinc deficient cells consistently demonstrated signs of increased immune activation and proinflammatory response compared to zinc adequate cells. Marginal zinc deficient cells repeatedly produced increased markers of immune activation and proinflammatory response as well, but to a lesser degree than more severely zinc deficient cells. The effect of zinc supplementation on immune function was not as clear. Zinc supplemented cells produced reduced levels of some of these markers and increased levels of other markers. These findings suggest that age-related zinc deficiency, which is similar to marginal zinc deficiency, may also have negative impacts on the immune system. Furthermore, our findings provide preliminary data for further cell culture studies or human trials of marginal zinc deficiency and zinc supplementation to further clarify their effects on the immune system.
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