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Impact of zinc on immune response

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Sabina Khanam at Yobe State University
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Impact of Zinc on Immune Response
Sabina Khanam*
Department of Biological Sciences, Yobe State University, Nigeria
*Corresponding author: Sabina Khanam, Department of Biological Sciences, Yobe State University, Nigeria, Tel: +234706336 6173; E-mail:
sabinakhanam@ymail.com
Received Date: July 5, 2018; Accepted Date: August 16, 2018; Published Date: August 23, 2018
Copyright: © 2018 Sabina Khanam. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Zinc is an essential element for various physiological activities in the body such as cell growth, cell differentiation
and development. It shows catalytic activity for various enzymes in both plants and animals. Zinc plays important
role in boosting the immune system by keeping immune system strong. Deficiency of zinc may affects the human
health and it causes many diseases such as hypogonadism, cognitive impairment, poor immune system, diarrhea,
delayed wound healing, oligospermia, neurosensory disorders, decreased body mass. Zinc deficiency mainly affects
T helper cells.
Keywords: Zinc; Immunity; Deciency; Physiology; Response
Introduction
Zinc is one of the most important trace elements on earth’s crust
which is essential for various cellular and catalytic activities of various
enzymes of the body for humans, plants and animals. Zinc is obtained
from various foods such as dairy products, poultry, eggs, legumes,
nuts, red meat, oysters, seafood, and cereals. It also plays very
important role in gene expression, protein synthesis, cell development,
nucleic acid synthesis, cell division, replication, growth and
development during pregnancy and from childhood to adolescence
and in immune function [1-6]. Zinc also known as immune booster by
increasing the body immunity because it functions as antioxidant. It
decreases oxidative stress markers and generation of inammatory
cytokines. It also helps in several physiological processes such as
digestion and regulation of hormone production in the endocrine
glands.
Severe deficiency Moderate deficiency Mild deficiency
Hypogonadism in males Growth retardation Oligospermia
Neurosensory disorders Poor appetite Decreased level of testosterone
Obsessive compulsive disorders Placental abruption Migraines
Weight loss Mental lethargy Hyperammonemia
Diarrhoea Male hypogonadism Decreased activity of thymulin
Psychological disorders Uterine dystocia Delayed puberty
Intercurrent infections due to cell-mediated immune
dysfunction Cell-mediated immune dysfunction Decreased activity of natural killer cells
Alopecia Neurosensory changes Decreased production of interleukin-2
Table 1: Zinc deciency and its eect on humans.
Zinc and Immune System
Many biological structures such as proteins, tissues and organs
protect against diseases comprising immune system. Immune system is
of two types: Innate immune system and Acquired immune system.
Innate immune system: It is a non-specic defence mechanism that
acts immediately when an antigen appears in the body.
Acquired immune system: Also known as adaptive immunity and it
is an antigen-specic immunity.
e most important cell in our body which protect from diseases is
white blood cells (WBC) or Leukocytes which destroy disease causing
substances. Zinc deciency may cause impaired immune function
which causes several types if infections in body such as
gastrointestinal, respiratory, inammatory diseases, autoimmune
disease and pneumonia. All these infections develop in the body
because level of inammatory cytokines (IL-6, IL-2, IL-1β) decreases
in the blood due to zinc deciency [7-9]. Zinc is essential element for
normal functioning of cells such as neutrophils and natural killer cells.
Zinc deciency also aects the normal development of acquired
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Immunology: Current Research Khanam, Immunol Curr Res 2018, 2:1
Short communication Open Access
Immunol Curr Res, an open access journal Volume 2 • Issue 1 • 1000104
immunity which is prevented by T lymphocytes and B lymphocytes in
our body by the activation of 1 cytokine production.
Conclusion
e purpose of this review is to study the relationship between zinc
and immunity. Zinc functions as a signalling molecule which targets
on specic molecule. Zinc deciency in the body alters the normal
functioning of immune system by altering the signalling pathways
which leads to various immunological disorders by aecting the T-cells
and B-cells.
References
1. Shah D, Sachdev HP (2001) Eect of gestational zinc deciency on
pregnancy outcomes: summary of observation studies and zinc
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2. Institute of Medicine, Food and Nutrition Board (2001) Dietary
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Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon,
Vanadium, and Zinc. Washington, DC: National Academy Press 442-501.
3. Prasad AS, Beck FW, Grabovski SM, Kaplan J, Mathog RH (1997) Zinc
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patients with head and neck cancer and in non-cancer subjects. Proc
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Paediatr Scand Suppl 319: 158-63.
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Citation: Sabina Khanam (2018) Impact of Zinc on Immune Response. Immunol Curr Res 2: 103.
Page 2 of 2
Immunol Curr Res, an open access journal Volume 2 • Issue 1 • 1000104
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Full-text available
  • Jul 2012
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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Zinc supplementation for the prevention of pneumonia in children aged 2 months to 59 months
Article
Full-text available
  • Dec 2010
Pneumonia is a leading cause of morbidity and mortality in children younger than five years of age. Most deaths occur during infancy and in low-income countries. Daily regimens of zinc have been reported to prevent acute lower respiratory tract infection and reduce child mortality. To evaluate the effectiveness of zinc supplementation in the prevention of pneumonia in children aged two to 59 months. We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2010, Issue 2), which contains the Acute Respiratory Infections Group's Specialised Register, MEDLINE (1966 to January Week 2, 2010), EMBASE (1974 to January 2010) and LILACS (1985 to January 2010). Randomised controlled trials (RCTs) evaluating supplementation of zinc for the prevention of pneumonia in children aged 2 to 59 months of age. Two review authors independently assessed trial quality and extracted data. We included six trials and 7850 participants in the meta-analysis. Analysis showed that zinc supplementation reduced the incidence of pneumonia by 13% (risk ratio (RR) 0.87; 95% confidence interval (CI) 0.81 to 0.94, fixed-effect, six studies) and prevalence of pneumonia by 41% (RR 0.59; 95% CI 0.35 to 0.99, random-effects, one study). On subgroup analysis, we found that zinc reduced the incidence of pneumonia defined by specific clinical criteria by 21% (i.e. confirmation by chest examination or chest radiograph) (RR 0.79; 95% CI 0.0.71 to 0.88, fixed-effect, four studies, n = 4591) but had no effect on lower specificity pneumonia case definition (i.e. age specific fast breathing with or without lower chest indrawing) (RR 0.95; 95% CI 0.86 to 1.06, fixed-effect, four studies, n = 3259). Zinc supplementation in children is associated with a reduction in the incidence and prevalence of pneumonia, the leading cause of death in children.
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Zinc in the Fetus and Newborn
Article
  • Feb 1985
  • Acta Paediatr Scand Suppl
The growing fetus and infant are at risk of becoming deficient of zinc, an adequate supply of which is essential for normal growth and development. Mild maternal zinc depletion was strongly associated with intrauterine growth retardation. Low levels of zinc in maternal plasma and poor placental perfusion reduced the materno-fetal transfer of zinc. Mean maternal dietary intake of zinc was 60% recommended daily allowance and mothers of small-for-gestational-age (SGA) babies consumed significantly less zinc than mothers of appropriate-for-gestational-age babies. In addition, iron/folate supplements, which are often routinely prescribed during pregnancy, despite dietary intakes of iron and folate being adequate, significantly decreased the oral bio-availability of zinc in pregnant women. Zinc supplementation may be beneficial to women at risk of delivering SGA babies. Zinc requirements and interactions are also important to consider when designing mineral supplements for preterm babies, infant formulae and food fortification in developing countries.
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Understanding zinc: Recent observations and interpretations
Article
  • Oct 1994
  • J Lab Clin Med
Zinc plays a key role in genetic expression, cell division, and growth and is essential for function of more than 200 enzymes. Effects of deficiency include stunting, anergy, dermatitis, poor healing, teratology, and neuropsychologic impairments. Risk of deficiency is related to level of anabolism and food choice. Bioavailability is greater from flesh foods than foods of plant origin. Pharmacologic intakes of zinc lower copper retention and impair copper-dependent processes. Pharmacologic intakes of folate impair zinc metabolism and may cause abnormal pregnancy outcomes. A recent review suggests zinc deficiency is common among populations of developing countries, particularly those that are deficient in iron.
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Zinc deficiency: Changes in cytokine production and T-cell subpopulations in patients with head and neck cancer and in noncancer subjects
Article
  • Feb 1997
Cell-mediated immune dysfunctions and susceptibility to infections have been observed in zinc-deficient human subjects. In this study, we investigated the production of cytokines and characterized the T-cell subpopulations in three groups of mildly zinc-deficient subjects. These included head and neck cancer patients, healthy volunteers who were found to have a dietary deficiency of zinc, and healthy volunteers in whom we induced zinc deficiency experimentally by dietary means. We used cellular zinc criteria for the diagnosis of zinc deficiency. We assayed enzyme-linked immunosorbent assay the production of cytokines from phytohemagglutinin-stimulated peripheral blood mononuclear cells and assessed by flow cytometry the differences in T-cell subpopulations. Our studies showed that the cytokines produced by TH1 cells were particularly sensitive to zinc status, inasmuch as the production of interleukin-2 (IL-2) and interferon-gamma were decreased even though the deficiency of zinc was mild in our subjects. TH2 cytokines (IL-4, IL-5, and IL-6) were not affected by zinc deficiency. Natural killer cell lytic activity also was decreased in zinc-deficient subjects. Recruitment of naive T cells (CD4+CD45 RA+) and CD8+ CD73+ CD11b-, precursors of cytolytic T cells, were decreased in mildly zinc-deficient subjects. An imbalance between the functions of TH1 and TH2 cells and changes in T-cell subpopulations are most probably responsible for cell-mediated immune dysfunctions in zinc deficiency.
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Human Zinc Deficiency
Article
  • Jun 2000
The objective of this paper is to provide a current overview of the significance of zinc in human nutrition. To achieve this, the following issues are addressed: (1) the biochemistry and biology of zinc in the context of their relevance to zinc in human nutrition and to our understanding of the complexity and practical importance of human zinc deficiency; (2) the history of our understanding of human zinc deficiency with an emphasis both on its brevity and on notable recent progress; (3) the clinical spectrum of severe zinc deficiency; (4) the lack of ideal biomarkers for milder zinc deficiency states, with the consequent dependence on randomized, placebo-controlled intervention studies to ascertain their prevalence and clinical consequences, including growth delay, diarrhea, pneumonia, other infections, disturbed neuropsychological performance and abnormalities of fetal development; (5) the public health significance of human zinc deficiency in the developing world; (6) reasons for concern and unanswered questions about zinc nutriture in the United States; (7) the need for better understanding of human zinc metabolism and homeostasis (including its limitations) at a molecular, cellular, organ-system and whole body level and of factors that affect zinc bioavailability; and (8) potential strategies for the prevention and management of human zinc deficiency. This review concludes with an emphasis on the immediate need for expanded research in directions that have become increasingly well demarcated and impelling as a result of recent progress, which is summarized in this overview.
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Effect of gestational zinc deficiency on pregnancy outcomes: Summary of observation studies and zinc supplementation trials
Article
  • Jun 2001
The lack of a valid indicator precludes a true estimate of zinc deficiency in pregnancy in various populations. However, it is possible that mild to moderate deficiency (as assessed by available indicators) may be common in the developing world. Animal experiments indicate that zinc deficiency can result in adverse maternal and fetal consequences. Human data, particularly from prenatal zinc supplementation trials, has failed to document a consistent maternal or infant benefit on evaluated outcome measures including pregnancy induced hypertension, preterm/post-term labour, premature rupture of membranes, maternal infection, postpartum haemorrhage, perinatal mortality, congenital malformations and fetal growth and gestation. Preliminary data suggest a beneficial effect of prenatal zinc supplementation on infants' neurobehavioural development and immune function (evaluated by diarrhoeal and ARI morbidity incidence in the first year of life). Future research should focus on these functional consequences and congenital malformations (with adequate sample sizes), and simultaneously address the safety issue, particularly in relation to micronutrient interactions. In the light of the currently available information, routine zinc supplementation can not be advocated to improve pregnancy outcome.
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Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic
  • Jan 2001
  • 442-501
Institute of Medicine, Food and Nutrition Board (2001) Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press 442-501.
Impact of Zinc on Immune Response
  • Jan 2018
  • 103
Citation: Sabina Khanam (2018) Impact of Zinc on Immune Response. Immunol Curr Res 2: 103.