The immune system is of import to an individual as it protects the body against infection and diseases that can affect normal body metabolisms. A healthy and well functioning immune system is dependent on the individual’s genetic makeup, diet, environmental factors, and a regular exercise program. The essence of dietary ingredients to the immune system is at the very foundation of the immune system: building it. Structural raw materials are derived from food ingested as well as the energy needed for the process (Raqib & Cravioto, 2009) Their role in the functioning of immune cells can further be ascertained on the effects that occur on the immune system when they are deficient (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009). The integrity of the immune response becomes compromised leading to increased probability of a patient succumbing to infectious diseases, cancer, suboptimal response to vaccinations, and other immunological disorders, e.g., allergies (Raqib & Cravioto, 2009). A wide range of dietary ingredients contribute to the integrity of the immune system. A few of them have been discussed in details in the following context
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1.1 Dietary factors that boost the immune system
1.1.1 Omega-3 polyunsaturated fatty acids (Omega-3 PUFA’s)
These groups of fatty acids are illustrious for their role in boosting immunity especially against cardiovascular diseases. They act by decreasing the production of inflammatory eicosanoids, cytokines, reactive oxygen species, and the expression of adhesion molecules (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009). Examples of Omega-3 PUFA’s include Eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and alpha-linolenic acid (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009). EPA and DHA can be found in oily fish and fish oils, while alpha-linolenic acid is found in walnuts (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009). EPA and DHA can either act directly by replacing arachidonic acid (AA) as an eicosanoid substrate and therefore inhibiting its metabolism, or indirectly by affecting the activation of the transcription factor and consequently altering the expression of inflammatory genes (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009). They also activate the production of inflammatory mediators termed resolvins (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009).
1.1.2. Antioxidant nutrients
These chemicals occur naturally in plant fruiting bodies, seeds, or root and, comprise of one or more phenol groups aimed at protecting the plant germline (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009). As a dietary component, antioxidants limit or control the immunopathology evoked by an immune response, by inhibiting the production of reactive oxygen species, produced by effector leukocytes.
Although normally needed in many metabolic and physiological processes due to their role as signaling molecules, in cases of inflammation, levels of reactive oxygen, nitrogen, and chlorine species exceed their normal levels in the blood resulting in a condition known as oxidative stress (Raqib & Cravioto, 2009). Oxidative stress can also be induced by unbalanced diets and aging and it renders the patient more vulnerable to cardiovascular diseases, including hypertension, atherosclerosis, myocardial infarction, diabetes, obesity, and cancer (Raqib & Cravioto, 2009). This condition can be forestalled by ingestion of antioxidants and trace elements either nutritionally or pharmacologically (Raqib & Cravioto, 2009). They have several mode of action including radical scavenging, interfering with the process of gene transcription, expression of protein, enzymatic activity, and metal chelation (Raqib & Cravioto, 2009).
Most antioxidants occur as micronutrients (e.g., vitamins C and E, selenium, and carotenoids) that are dependent upon diet-derived micronutrients (e.g., Cu-Zn and Mn superoxide dismutase) (Raqib & Cravioto, 2009). Some are however produced by specific endogenous pathways (catalase, superoxide dismutase and glutathione peroxidase, and glutathione S-transferase) (Raqib & Cravioto, 2009). Some antioxidants act directly (e.g., plant metabolite and flavonoids); while others (as pro-antioxidants, e.g., phytochemicals) act by counteracting the damaging effects of reactive species, either by modulation of direct agents or by regulation of the biosynthesis of antioxidant proteins (Raqib & Cravioto, 2009). Some of the day to day foods we take that contain antioxidants include grapes, apples, berries, pomegranates, green tea, and many others (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009). There is also scientific evidence supporting the fact that consuming vegetables and fruits in plenty or a diet rich in antioxidants, serum carotenoids, vitamins, fiber, and magnesium are beneficial in terms of reducing inflammation and in particular CRP levels (Warnberg, Gomez-Martinez, Romeo, Diaz, & Marcos, 2009).
1.1.3 Trace elements
Iron as a micronutrient is a requisite for the proper functioning of neutrophils and NK cell-mediated killing and T-cell proliferative responses (Jones, Berkley, & Warner, 2010). Iron deficiency has been illustrated to orchestrate the immune response towards the Th2 type (Jones, Berkley, & Warner, 2010). However, in some instances, the body deprives itself of iron as a mechanism for pathogen elimination since the pathogens also need the element for proliferation (Jones, Berkley, & Warner, 2010). Iron should therefore be taken in very low level in people living in malaria endemic areas but for those living outside these areas, especially populations with high levels of anemia, routine supplementation is recommended (Jones, Berkley, & Warner, 2010). Iron supplements should be taken when necessary and should be accompanied by institution or broad spectrum antibiotics to compensate for the increased susceptibility to pathogen attacks (Jones, Berkley, & Warner, 2010).
Zinc plays an essential role in the growth, development and functioning of the cells of the immune system (Cummins & Kovacic, 2009). One of its main principal functions in the immune system is the activation of some immunity mediators e.g. thymulin (Cummins & Kovacic, 2009). Thymulin is a nonapeptidic hormone secreted by thymic epithelial cells which promotes T lymphocyte maturation, cytotoxicity, and IL-2 production (Cummins & Kovacic, 2009). The activeness of thymulin, in vitro and in vivo, in both animals and humans, depends on plasmic zinc levels such that although detectable in patients with zinc deficiency, it occurs in an inactive state (Cummins & Kovacic, 2009).
Zinc is also a chief requirement in cytokine activity by inhibiting the production of TH1 cells causing a shift in the TH1-TH2 balance (Cummins & Kovacic, 2009). Zinc deficiency affects the production and/or activity of IL-1, IL-2, IL-3, IL-4, IL-6, IFN-g and TNF-a (Cummins & Kovacic, 2009). Its role in the stabilization of membranes is illustrated on the effects zinc deficiency on phagocytosis, oxygen consumption and bactericidal activity of phagocytic cells and the modification of ConA surface receptor on lymphoid cells (Cummins & Kovacic, 2009). In addition to the above functions, zinc is a key prerequisite in lymphocyte apoptosis in vitro and in vivo (Cummins & Kovacic, 2009). Its deficiency relative to this role causes thymic atrophy and lymphopenia ascribable to alteration in lymphocyte production, and the loss of precursor cells thru an apoptotic mechanism (Cummins & Kovacic, 2009).
Although it is known to be essential to the proper functioning of the immune system, its mode of action is not clearly known (Arthur, McKenizie, & Beckett, 2003). It has been essayed for its influence on both the innate, and the acquired immune systems (Arthur, McKenizie, & Beckett, 2003). Lymphocytes that have selenium deficiency have less ability to proliferate in response to mitogen while in macrophages the deficiency affects leukotriene B4 synthesis, an important process in neutrophil chemotaxis (Arthur, McKenizie, & Beckett, 2003). The humoral system also depends on selenium levels sufficient production of IgG and IgM titers (Arthur, McKenizie, & Beckett, 2003). Asthmatic patients also present with selenium deficiency in their endothelial cells (Arthur, McKenizie, & Beckett, 2003). Consequently, there is an increase in expression of adhesion molecules, which causes greater adhesion of neutrophils. (Arthur, McKenizie, & Beckett, 2003)
188.8.131.52 Vitamin A
Vitamin A has a diverse range of roles in effective immune responses especially in the maintenance of the integrity of mucosal surfaces (Jones, Berkley, & Warner, 2010). This is the basic reason why patients with deficiency in Vitamin A present with increased rates of invasive infections in the respiratory system, gastrointestinal tract and the ocular (Jones, Berkley, & Warner, 2010). Vitamin A is also significant in phagocytic cells and NK cell function, and with both Th1 and, especially, Th2 responses (Jones, Berkley, & Warner, 2010).
184.108.40.206. Vitamin C and E
It has been essayed that a single dose of Vitamin C has the ability to suppress primary abnormalities in neutrophil motility and antimicrobial activity in humans with chronic granulomatous disease (Erickson, Medina, & Hubbard, 2000). Neutrophil mobility has also been proven to improve in patients with bronchial asthma (Erickson, Medina, & Hubbard, 2000). The vitamins also increase neutrophil adherence, chemotaxis, and phagocytic capacity even though they decreased superoxide production by neutrophils (Erickson, Medina, & Hubbard, 2000). Healthy individuals who take vitamin C and E as supplements present suppressed neutrophil production of oxygen free radicals hence presenting antioxidant effects (Erickson, Medina, & Hubbard, 2000). Vitamin C inhibits the activation of the oxidant-sensitive transcription factor NF-kB, which mediates the production of proinflammatory cytokines such as IL-1 and TNF-a (Erickson, Medina, & Hubbard, 2000).
220.127.116.11. Vitamin D
Vitamin D has a wide range of immunological benefits ranging from promotion of Th2 and regulatory T-cell signaling, to increasing the antimycobacterial properties of monocytes and macrophages (Erickson, Medina, & Hubbard, 2000). Vitamin D deficiency manifests itself as increased susceptibility to respiratory tract infections, and recently, pneumonia (Erickson, Medina, & Hubbard, 2000). Before antibiotics were contrived, Vitamin D served as the main treatment for tuberculosis and recently, Vitamin B is being incorporated in TB treatment (Erickson, Medina, & Hubbard, 2000).