Zinc deficiency induces production of the proinflammatory cytokines IL-1β and TNFα in promyeloid cells via epigenetic and redox-dependent mechanisms

Weßels, Inga; Haase, Hajo; Engelhardt, Gabriela; Rink, Lothar; Uciechowski, Peter

doi:10.1016/j.jnutbio.2012.06.007

Cited by 124 publications

(92 citation statements)

References 48 publications

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“…This was seen in LPS-stimulated PBMCs from zinc-deficient adults compared to their zinc-sufficient counterparts [71]. This observation was confirmed through studying the epigenetic mechanisms that are implicated during zinc deficiency and it was reported that long term zinc deprivation promoted changes of the chromatin structures of IL-1β and TNFα promoters enabling the expression of both genes [72]. Additionally, phytohaemagglutinin (PHA)-induced production of IL-2 was reduced in PBMCs of zinc-deficient patients with head and neck cancer and in zinc-deficient healthy volunteers [73].…”

Section: Zinc Status and Inflammatory Cytokinesmentioning

confidence: 55%

Zinc in Infection and Inflammation

Gammoh¹,

Rink²

2017

Preprint

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187

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Abstract:Micronutrient homeostasis is a key factor in maintaining a healthy immune system. Zinc is an essential micronutrient that is involved in the regulation of the innate and adaptive immune responses. The main cause of zinc deficiency is malnutrition. Zinc deficiency leads to cell-mediated immune dysfunctions among other manifestations. Consequently, such dysfunctions lead to a worse outcome in the response towards bacterial infection and sepsis. For instance, zinc is an essential component of the pathogen-eliminating signal transduction pathways leading to neutrophil extracellular traps formation, as well as inducing cell-mediated immunity over humoral immunity by regulating specific factors or differentiation. Additionally, zinc deficiency plays a role in inflammation, mainly elevating inflammatory response as well as damage to host tissue. Zinc is involved in the modulation of the proinflammatory response by targeting Nuclear Factor Kappa B, a transcription factor that is the master regulator of proinflammatory responses. It is also involved in controlling oxidative stress and regulating inflammatory cytokines. Zinc plays an intricate function during an immune response and its homeostasis is critical for sustaining proper immune function. This review will summarize the latest findings concerning the role of this micronutrient during the course of infections and inflammatory response and how the immune system modulates zinc depending on different stimuli.

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Section: Zinc Status and Inflammatory Cytokinesmentioning

confidence: 55%

Zinc in Infection and Inflammation

Gammoh¹,

Rink²

2017

Preprint

Self Cite

187

139

View full text Add to dashboard Cite

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“…13 The supernatants of the samples for the phagocytosis/ burst assays were retained and used for washing-and incubation steps in the FluoZin-3 assay, to avoid contact with media or buffer with normal Zn 2+ content.…”

Section: Flow Cytometric Measurement Of Intracellular Free Zinc Ionsmentioning

confidence: 99%

Differential impact of zinc deficiency on phagocytosis, oxidative burst, and production of pro-inflammatory cytokines by human monocytes

et al. 2014

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Zinc deficiency has a fundamental influence on the immune defense, with multiple effects on different immune cells, resulting in a major impairment of human health. Monocytes and macrophages are among the immune cells that are most fundamentally affected by zinc, but the impact of zinc on these cells is still far from being completely understood. Therefore, this study investigates the influence of zinc deficiency on monocytes of healthy human donors. Peripheral blood mononuclear cells, which include monocytes, were cultured under zinc deficient conditions for 3 days. This was achieved by two different methods:by application of the membrane permeable chelator N,N,N 0 ,N 0 -tetrakis-(2-pyridylmethyl)ethylenediamine (TPEN) or by removal of zinc from the culture medium using a CHELEX 100 resin. Subsequently, monocyte functions were analyzed in response to Escherichia coli, Staphylococcus aureus, and Streptococcus pneumoniae. Zinc depletion had differential effects. On the one hand, elimination of bacterial pathogens by phagocytosis and oxidative burst was elevated. On the other hand, the production of the inflammatory cytokines tumor necrosis factor (TNF)-a and interleukin (IL)-6 was reduced. This suggests that monocytes shift from intercellular communication to basic innate defensive functions in response to zinc deficiency.These results were obtained regardless of the method by which zinc deficiency was achieved. However, CHELEX-treated medium strongly augmented cytokine production, independently from its capability for zinc removal. This side-effect severely limits the use of CHELEX for investigating the effects of zinc deficiency on innate immunity.

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“…Although there were improvements in time spent finding a hidden platform in the Morris Water Maze (MWM), a test that examines spatial learning and memory, in rats given the zinc-supplemented diet alone after injury, an early zinc injection alone did not enhance MWM performance [8 & ]. Together these data strongly suggest that zinc status should be monitored and maintained after a brain injury, not only because of the reported neurocognitive outcomes, but also because both zinc deficiency and TBI have been associated with oxidative stress [9,10] …”

Section: Traumatic Brain Injury and The Development Of Zinc Deficiencymentioning

confidence: 87%