T-helper type 1 cytokine release is enhanced by in vitro zinc supplementation due to increased natural killer cells

Metz, Claudia H.D.; Schröder, AC; Overbeck, Silke; Kahmann, Laura; Plümäkers, Birgit; Rink, Lothar

doi:10.1016/j.nut.2006.10.007

Cited by 37 publications

(20 citation statements)

References 35 publications

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“…Cell culture studies using primary human cells demonstrate effects of zinc on cytokines that differ according to the zinc concentration and activation state of the cell (Table 3) [50,51,52,53,54,55,56]. Zinc treatment enhanced IFN-γ & IL-10 concentrations in PHA-stimulated PBMC [50] and IL-1β & TNF-α in LPS-stimulated cells, while zinc down-regulated levels of IL-1β & TNF-α in PBMC stimulated with superantigens [55].…”

Section: Zinc Status and Cytokinesmentioning

confidence: 99%

Zinc and Regulation of Inflammatory Cytokines: Implications for Cardiometabolic Disease

2012

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In atherosclerosis and diabetes mellitus, the concomitant presence of low-grade systemic inflammation and mild zinc deficiency highlights a role for zinc nutrition in the management of chronic disease. This review aims to evaluate the literature that reports on the interactions of zinc and cytokines. In humans, inflammatory cytokines have been shown both to up- and down-regulate the expression of specific cellular zinc transporters in response to an increased demand for zinc in inflammatory conditions. The acute phase response includes a rapid decline in the plasma zinc concentration as a result of the redistribution of zinc into cellular compartments. Zinc deficiency influences the generation of cytokines, including IL-1β, IL-2, IL-6, and TNF-α, and in response to zinc supplementation plasma cytokines exhibit a dose-dependent response. The mechanism of action may reflect the ability of zinc to either induce or inhibit the activation of NF-κB. Confounders in understanding the zinc-cytokine relationship on the basis of in vitro experimentation include methodological issues such as the cell type and the means of activating cells in culture. Impaired zinc homeostasis and chronic inflammation feature prominently in a number of cardiometabolic diseases. Given the high prevalence of zinc deficiency and chronic disease globally, the interplay of zinc and inflammation warrants further examination.

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Section: Zinc Status and Cytokinesmentioning

confidence: 99%

Zinc and Regulation of Inflammatory Cytokines: Implications for Cardiometabolic Disease

2012

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“…Zinc has a direct effect ( Fig. 1) on the stimulation of thymus, naïve T cell production, clonal expansion, Th1/Th2 cell differentiation and Th1 T cell stimulation [37,38]. Zinc deficiency in murine models has been shown to be associated with thymic atrophy, decreased splenocyte counts and blunted response to all antigens-T-cell dependent as well as independent [39].…”

Section: Zinc and Immunitymentioning

confidence: 99%

Roles of Zinc in the Pathophysiology of Acute Diarrhea

Kulkarni

Mamtani

Patel

2011

Curr Infect Dis Rep

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Zinc has caught wide scientific attention for the conceptual promise it has to offer for prevention, control and treatment of acute diarrhea. This review focuses on the mechanisms by which zinc might contribute to the pathogenesis of acute diarrhea and the degree of success achieved in diarrhea control and treatment by zinc supplementation. Animal and in vitro studies have continued to fascinate the scientific fraternity and form a solid basis for the potential use of zinc supplementation against diarrhea. However, emerging evidence in terms of controlled studies in humans beckons a more complete understanding of the mechanistic basis for zinc supplementation. Current evidence indicates that studies specifically addressing the variability in response to zinc supplementation need to be undertaken to better comprehend these mechanisms.

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“…Two phenotypically distinct T-lymphocyte populations have been identified that are zinc-sensitive: the Th1 response, important in protecting against intracellular infections and the Th2 response, important in protecting against noninvasive infections such as helminths. Adequate zinc and energy intake leads to a dominant Th1 response and a downregulated Th2 response, whereas inadequate intake of zinc and energy activates the Th2 response and downregulates the Th1 response [13,14 ]. An upregulated Th1 response is more protective against many of the invasive diarrheal pathogens such as Shigella spp.…”

Section: Zinc and The Immune Systemmentioning

confidence: 99%

Zinc and diarrheal disease: current status and future perspectives

Scrimgeour

Lukaski

2008

Current Opinion in Clinical Nutrition and Metabolic Care

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Faced with rising antibiotic resistance and the lack of effective antidiarrheal vaccines, oral zinc provides substantial benefit in the reduction of stool output and disease duration combined with safety, selectivity of action, and low cost. Thus, oral zinc supplementation is a practical therapeutic intervention for the treatment of diarrhea in children, and by extension, should be provided to adults.

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T-helper type 1 cytokine release is enhanced by in vitro zinc supplementation due to increased natural killer cells

Cited by 37 publications

References 35 publications

Zinc and Regulation of Inflammatory Cytokines: Implications for Cardiometabolic Disease

Zinc and Regulation of Inflammatory Cytokines: Implications for Cardiometabolic Disease

Roles of Zinc in the Pathophysiology of Acute Diarrhea

Zinc and diarrheal disease: current status and future perspectives

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