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

Mayer, Lena; Uciechowski, Peter; Meyer, Sören; Schwerdtle, Tanja; Rink, Lothar; Haase, Hajo

doi:10.1039/c4mt00051j

Cited by 77 publications

(61 citation statements)

References 38 publications

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“…The intracellular distribution of zinc might lead additionally to effective clearance of the intracellular pathogen. 47 This is in accordance with the fact that the presence of zinc is able to inhibit NADPH oxidase with subsequent inhibition of ROS production. In particular, impaired lymphopoiesis was seen in zinc-deficient mice, whereas the numbers of monocytes and neutrophils increased.…”

Section: Antioxidant Effects Of Zinc Within Immune Cellssupporting

confidence: 76%

Zinc as a micronutrient and its preventive role of oxidative damage in cells

2015

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Zinc is an essential trace element with special importance in the immune system. Deficiencies of zinc are seen in the course of ageing and in various diseases, such as diabetes mellitus or rheumathoid arthritis. The trace element is essential for a variety of basic cellular functions and especially important for various enzymes participating in the production and neutralization of reactive oxygen species (ROS) which are normally produced by the cell. Under normal conditions ROS are neutralized and are not able to harm the cell, but in case of ROS elevation, oxidative damage within the cell is the result. Interestingly, zinc deficiency is directly associated with oxidative stress. Thus, control and regulation of the intracellular zinc content is essential with participation of various transporter and zinc-binding proteins, such as metallothionein. Oxidative stress is mainly caused by elevated ROS production and a decrease of antioxidant mechanisms. Zinc partly functions as an antioxidant although it is redox inert. Zinc supplementation is associated with decreased ROS formation exhibiting beneficial effects especially in ageing and diabetes mellitus. This review summarizes current findings concerning zinc as a micronutrient and its actions as a pro-antioxidant, and the association between zinc and oxidative stress under various conditions is highlighted.

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Section: Antioxidant Effects Of Zinc Within Immune Cellssupporting

confidence: 76%

Zinc as a micronutrient and its preventive role of oxidative damage in cells

2015

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“…Preclinical models as well as human translational studies have demonstrated that low serum zinc concentrations may exacerbate inflammation through disruption of epithelial barrier function, impaired mucosal immunity, and increasing pro-inflammatory cytokines (2) (9) (11) (12) (13, 14). Lending support to the outcomes of these mechanistic investigations, a recently published prospective study examining 17,776 healthy women who were followed over a 26-year period reported that dietary zinc supplementation was inversely associated with the risk being diagnosed with Crohn’s disease (15).…”

Section: Discussionmentioning

confidence: 99%

Zinc Deficiency is Associated with Poor Clinical Outcomes in Patients with Inflammatory Bowel Disease

Siva

Rubin

Gulotta

et al. 2017

Inflammatory Bowel Diseases

124

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Introduction Zinc plays a pivotal role in wound repair, tissue regeneration, and the immune response. Although zinc deficiency is common in patients with inflammatory bowel disease (IBD), the impact of low serum zinc levels on disease course is not known. Methods Patients enrolled in a prospectively collected IBD registry with at least two serum zinc measurements were included in the analysis. Using a logistic regression model, rates of IBD-related surgeries, IBD-related hospitalizations, and IBD-related complications were evaluated following a diagnosis of zinc deficiency (serum concentration <0.66 mcg/ml) compared to those with normal zinc concentrations. In patients who were zinc deficient, outcomes were also analyzed between those who had normalization of zinc levels within 12 months and those who remained deficient. Results A total of 773 patients with Crohn’s disease (CD) and 223 with ulcerative colitis (UC) were included in the analysis. After adjusting for covariates, zinc deficiency was associated with an increased risk of subsequent hospitalizations, surgeries, and disease-related complications in patients with CD and UC (CD: hospitalizations, OR 1.44, 95% CI [1.02-2.04]; surgeries, 2.05 [1.38-3.05]; complications, 1.50 [1.04-2.15]; UC: hospitalizations, 2.14 [1.07-4.29]; surgeries, 1.64 [0.59-4.52]; complications, 1.97 [0.94-4.11]). Normalization of zinc was associated with improvement in these outcomes in patients with both CD and UC. Conclusion IBD patients with serum zinc deficiency are more likely to have adverse disease-specific outcomes. As these outcomes improve with normalization of zinc, the results from this study support the role for close monitoring and replacement of zinc in patients with IBD.

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“…However, monocytes and macrophages are more resistant to zinc deficiency and high zinc levels [20]. In the central nervous system (CNS), the effect of zinc administration on neuroinflammation has not yet been completely characterized especially following cerebral ischemia.…”

Section: Introductionmentioning

confidence: 99%

Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model

Tomás-Sanchez

Blanco-Álvarez

González-Barrios

et al. 2016

Journal of Immunology Research

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Acute and subacute administration of zinc exert neuroprotective effects in hypoxia-ischemia animal models; yet the effect of chronic administration of zinc still remains unknown. We addressed this issue by injecting zinc at a tolerable dose (0.5 mg/kg weight, i.p.) for 14 days before common carotid artery occlusion (CCAO) in a rat. After CCAO, the level of zinc was measured by atomic absorption spectrophotometry, nitrites were determined by Griess method, lipoperoxidation was measured by Gerard-Monnier assay, and mRNA expression of 84 genes coding for cytokines, chemokines, and their receptors was measured by qRT-PCR, whereas nitrotyrosine, chemokines, and their receptors were assessed by ELISA and histopathological changes in the temporoparietal cortex-hippocampus at different time points. Long-term memory was evaluated using Morris water maze. Following CCAO, a significant increase in nitrosative stress, inflammatory chemokines/receptors, and cell death was observed after 8 h, and a 2.5-fold increase in zinc levels was detected after 7 days. Although CXCL12 and FGF2 protein levels were significantly increased, the long-term memory was impaired 12 days after reperfusion in the Zn+CCAO group. Our data suggest that the chronic administration of zinc at tolerable doses causes nitrosative stress, toxic zinc accumulation, and neuroinflammation, which might account for the neuronal death and cerebral dysfunction after CCAO.

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

Cited by 77 publications

References 38 publications

Zinc as a micronutrient and its preventive role of oxidative damage in cells

Zinc as a micronutrient and its preventive role of oxidative damage in cells

Zinc Deficiency is Associated with Poor Clinical Outcomes in Patients with Inflammatory Bowel Disease

Prophylactic Chronic Zinc Administration Increases Neuroinflammation in a Hypoxia-Ischemia Model

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