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How The Immune System ACTUALLY Works – IMMUNEAc and immune system function -
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Qin C, Zhou L, Hu Z, Zhang S, Yang S, Tao Y, et al. Dysregulation of immune response in patients with coronavirus COVID in Wuhan, China. Diao B, Wang C, Tan Y, Chen X, Liu Y, Ning L, et al. Reduction and functional exhaustion of T cells in patients with coronavirus disease COVID Citation: Alagawany M, Attia YA, Farag MR, Elnesr SS, Nagadi SA, Shafi ME, Khafaga AF, Ohran H, Alaqil AA and Abd El-Hack ME The Strategy of Boosting the Immune System Under the COVID Pandemic.
Received: 08 June ; Accepted: 24 August ; Published: 08 January Copyright © Alagawany, Attia, Farag, Elnesr, Nagadi, Shafi, Khafaga, Ohran, Alaqil and Abd El-Hack.
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Check for updates. REVIEW article. The Strategy of Boosting the Immune System Under the COVID Pandemic Mahmoud Alagawany 1 Youssef A.
Farag 5 Shaaban S. Elnesr 6 Sameer A. Nagadi 2 Manal E. Shafi 7 Asmaa F. Khafaga 8 Husein Ohran 9 Abdulaziz A. Alaqil 10 Mohamed E. Introduction Coronaviridae is one of the families of viruses that are known to cause diseases in birds and mammals ranging from the common cold to severe acute respiratory syndrome SRAS.
Symptoms and Risk Factors of COVID Two to 14 days after exposure to the virus, the usual clinical signs are dry cough and shortness of breath. Figure 2. The role of vitamin C in the immune defense.
Table 1. The immune functions and mechanisms of vitamins. Table 2. The immune functions and mechanisms of minerals. m PubMed Abstract CrossRef Full Text Google Scholar.
Supplementation with 1. In addition to PUFAs, isomers of LA called conjugated linoleic acid CLA have been shown to modulate immune function, mainly in animal and in vitro studies CLA is found naturally in meat and milk of ruminant animals, but it is also available as a dietary supplement that contains two isomers, cis -9, trans CLA and trans , cis CLA.
CLA supplementation was also associated with a decrease in levels of two pro-inflammatory cytokines and an increase in levels of an anti-inflammatory cytokine Similar effects on the immune response have been observed in some animal studies 47, 48 ; however, a few other human studies have not found beneficial effects of CLA on various measures of immune status and function More research is needed to understand the effects of CLA on the human immune response.
Further, lipids in general have a number of other roles in immunity besides being the precursors of eicosanoids and similar immune mediators.
For instance, lipids are metabolized by immune cells to generate energy and are also important structural and functional components of cell membranes. Moreover, lipids can regulate gene expression through stimulation of membrane receptors or through modification of transcription factor activity.
Further, lipids can covalently modify proteins , thereby affecting their function Deficiencies in select micronutrients vitamins and nutritionally essential minerals can adversely affect aspects of both innate and adaptive immunity, increasing vulnerability to infection and disease.
Micronutrient deficiencies are quite common in the general US population, but especially in the poor, the elderly, and those who are obese see Overnutrition and obesity 52, Moreover, vitamin D deficiency is a major problem in the US and elsewhere; it has been estimated that 1 billion people in the world have either vitamin D deficiency or insufficiency Because micronutrients play crucial roles in the development and expression of immune responses, selected micronutrient deficiencies can cause immunosuppression and thus increased susceptibility to infection and disease.
The roles of several micronutrients in immune function are addressed below. Vitamin A and its metabolites play critical roles in both innate and adaptive immunity.
In innate immunity, the skin and mucosal cells of the eye and respiratory, gastrointestinal , and genitourinary tracts function as a barrier against infections. Vitamin A helps to maintain the structural and functional integrity of these mucosal cells.
Vitamin A is also important to the normal function of several types of immune cells important in the innate response, including natural killer NK cells , macrophages , and neutrophils. Moreover, vitamin A is needed for proper function of cells that mediate adaptive immunity, such as T and B lymphocytes ; thus, vitamin A is necessary for the generation of antibody responses to specific antigens Most of the immune effects of vitamin A are carried out by vitamin A derivatives, namely isomers of retinoic acid.
Isomers of retinoic acid are steroid hormones that bind to retinoid receptors that belong to two different classes: retinoic acid receptors RARs and retinoid X receptors RXRs.
In the classical pathway, RAR must first heterodimerize with RXR and then bind to small sequences of DNA called retinoic acid response elements RAREs to initiate a cascade of molecular interactions that modulate the transcription of specific genes More than genes are directly or indirectly regulated by retinoic acid Several of these genes control cellular proliferation and differentiation ; thus, vitamin A has obvious importance in immunity.
Vitamin A deficiency is a major public health problem worldwide, especially in developing nations, where availability of foods containing preformed vitamin A is limited for information on sources of vitamin A, see the article on Vitamin A.
Experimental studies in animal models, along with epidemiological studies , have shown that vitamin A deficiency leads to immunodeficiency and increases the risk of infectious diseases In fact, deficiency in this micronutrient is a leading cause of morbidity and mortality among infants, children, and women in developing nations.
Vitamin A-deficient individuals are vulnerable to certain infections, such as measles, malaria , and diarrheal diseases Subclinical vitamin A deficiency might increase risk of infection as well Infections can, in turn, lead to vitamin A deficiency in a number of different ways, for example, by reducing food intake, impairing vitamin absorption, increasing vitamin excretion , interfering with vitamin utilization, or increasing metabolic requirements of vitamin A Many of the specific effects of vitamin A deficiency on the immune system have been elucidated using animal models.
Vitamin A deficiency impairs components of innate immunity. As mentioned above, vitamin A is essential in maintaining the mucosal barriers of the innate immune system.
Thus, vitamin A deficiency compromises the integrity of this first line of defense, thereby increasing susceptibility to some types of infection, such as eye, respiratory, gastrointestinal , and genitourinary infections Vitamin A deficiency results in reductions in both the number and killing activity of NK cells, as well as the function of neutrophils and other cells that phagocytose pathogens like macrophages.
Specific measures of functional activity affected appear to include chemotaxis , phagocytosis , and immune cell ability to generate oxidants that kill invading pathogens In addition, cytokine signaling may be altered in vitamin A deficiency, which would affect inflammatory responses of innate immunity.
Additionally, vitamin A deficiency impairs various aspects of adaptive immunity, including humoral and cell-mediated immunity. In particular, vitamin A deficiency negatively affects the growth and differentiation of B cells, which are dependent on retinol and its metabolites 68, Vitamin A deficiency also affects B cell function; for example, animal experiments have shown that vitamin A deficiency impairs antibody responses With respect to cell-mediated immunity, retinol is important in the activation of T cells 73 , and vitamin A deficiency may affect cell-mediated immunity by decreasing the number or distribution of T cells, altering cytokine production, or by decreasing the expression of cell-surface receptors that mediate T-cell signaling Vitamin A supplementation enhances immunity and has been shown to reduce the infection-related morbidity and mortality associated with vitamin A deficiency.
Vitamin A supplementation of mothers during pregnancy or lactation , and early infants months does not appear to significantly affect child mortality, while supplementation of neonates 0 to 28 days may reduce childhood mortality at 6 months of age 77, Vitamin A supplementation is not beneficial in those with lower respiratory infections, such as pneumonia 77 , and supplementation may actually aggravate the condition 56 , Although the effectiveness of vitamin A supplementation in children older than 6 months of age in low- and middle-income countries is now well established, the most effective dose and frequency of supplemental vitamin A delivery is still a matter of debate 56 , 74 , For more information on vitamin A supplementation and childhood morbidity and mortality, see the article on Vitamin A.
Because of potential adverse effects, vitamin A supplements should be reserved for undernourished populations and those with evidence of vitamin A deficiency For information on vitamin A toxicity, see the article on Vitamin A.
Like vitamin A, the active form of vitamin D , 1,dihydroxyvitamin D 3 , functions as a steroid hormone to regulate expression of target genes. Many of the biological effects of 1,dihydroxyvitamin D 3 are mediated through a nuclear transcription factor known as the vitamin D receptor VDR Upon entering the nucleus of a cell, 1,dihydroxyvitamin D 3 associates with the VDR and promotes its association with the retinoid X receptor RXR.
In addition to its effects on mineral homeostasis and bone metabolism , 1,dihydroxyvitamin D 3 is now recognized to be a potent modulator of the immune system. The VDR is expressed in several types of immune cells, including monocytes , macrophages , dendritic cells , and activated T cells Macrophages also produce the hydroxyvitamin D 3 hydroxylase enzyme , allowing for local conversion of vitamin D to its active form Studies have demonstrated that 1,dihydroxyvitamin D 3 modulates both innate and adaptive immune responses.
Antimicrobial peptides AMPs and proteins are critical components of the innate immune system because they directly kill pathogens , especially bacteria , and thereby enhance immunity AMPs also modulate immune functions through cell-signaling effects The active form of vitamin D regulates two important antimicrobial proteins, cathelicidin and defensin Vitamin D has also been shown to stimulate other components of innate immunity, including immune cell proliferation and cytokine production Through these roles, vitamin D helps protect against infections caused by pathogens.
Vitamin D has mainly inhibitory effects on adaptive immunity. In particular, 1,dihydroxyvitamin D 3 suppresses antibody production by B cells and also inhibits proliferation of T cells in vitro Moreover, 1,dihydroxyvitamin D 3 has been shown to modulate the functional phenotype of helper T cells and dendritic cells T cells that express the cell-surface protein CD4 are divided into two subsets depending on the particular cytokines that they produce: T helper Th 1 cells are primarily involved in activating macrophages and inflammatory responses, and Th2 cells are primarily involved in stimulating antibody production by B cells 4.
Some studies have shown that 1,dihydroxyvitamin D 3 inhibits the development and function of Th1 cells 99, but enhances the development and function of Th2 cells , and regulatory T cells , Because these latter cell types are important regulators in autoimmune disease and graft rejections, vitamin D is suggested to have utility in preventing and treating such conditions Studies employing various animal models of autoimmune diseases and transplantation have reported beneficial effects of 1,dihydroxyvitamin D 3 reviewed in Indeed, vitamin D deficiency has been implicated in the development of certain autoimmune diseases, such as insulin-dependent diabetes mellitus IDDM; type 1 diabetes mellitus , multiple sclerosis MS , systemic lupus erythematosis SLE , and rheumatoid arthritis RA.
Autoimmune diseases occur when the body mounts an immune response against its own tissue instead of a foreign pathogen.
The targets of the inappropriate immune response are the insulin -producing β-cells of the pancreas in IDDM, the myelin -producing cells of the central nervous system in MS, multiple tissues and organs in SLE, and the collagen -producing cells of the joints in RA , Several case-control studies have found low serum hydroxyvitamin D 3 concentrations in individuals with IDDM, MS, and SLE; among these individuals, lower serum hydroxyvitamin D 3 concentrations have been associated with increased disease activity and relapse rates Both genetic factors e.
For example, some observational studies have found the prevalence of various autoimmune conditions increases as latitude increases , This suggests that lower exposure to ultraviolet-B radiation the type of radiation needed to induce vitamin D synthesis in skin and the associated decrease in endogenous vitamin D synthesis may play a role in the pathology of autoimmune diseases.
Low vitamin D intake has also been associated with an increased risk of MS , IDDM , and RA Despite the well-documented relationship between low vitamin D status and autoimmune disease, few randomized controlled trials RCTs have been conducted, and the clinical efficacy of vitamin D supplementation in autoimmune prevention and treatment remains uncertain A meta-analysis of RCTs that tested the effect of high-dose vitamin D supplements on the risk of relapse in MS patients included only five RCTs with a total of patients and controls and found no significant effect A systematic review similarly reported no effect of vitamin D supplementation on MS relapse At this time, we await the results of three ongoing RCTs evaluating the efficacy of vitamin D supplementation on disease progression and activity in individuals with relapsing remitting MS For more information on the specific autoimmune conditions discussed above, see the article on Vitamin D.
Primarily through this role, the vitamin affects several components of innate and adaptive immunity; for example, vitamin C has been shown to stimulate both the production and function , of leukocytes white blood cells , especially neutrophils , lymphocytes , and phagocytes.
Specific measures of functions stimulated by vitamin C include cellular motility , chemotaxis , , and phagocytosis Neutrophils, which attack foreign bacteria and viruses , seem to be the primary cell type stimulated by vitamin C, but lymphocytes and other phagocytes are also affected Additionally, several studies have shown that supplemental vitamin C increases serum levels of antibodies , and C1q complement proteins in guinea pigs, which — like humans — cannot synthesize vitamin C and hence depend on dietary vitamin C.
However, some studies have reported no beneficial changes in leukocyte production or function with vitamin C treatment Vitamin C may also protect the integrity of immune cells.
Neutrophils, mononuclear phagocytes, and lymphocytes accumulate vitamin C to high concentrations, which can protect these cell types from oxidative damage , , Vitamin C, through its antioxidant functions, has been shown to protect leukocytes from such effects of autooxidation Phagocytic leukocytes also produce and release cytokines , including interferons that have antiviral activity Vitamin C has been shown to increase interferon levels in vitro Further, vitamin C regenerates the antioxidant vitamin E from its oxidized form It is widely thought by the general public that vitamin C boosts the function of the immune system, and accordingly, may protect against viral infections and perhaps other diseases.
While some studies suggest the biological plausibility of vitamin C as an immune enhancer, human studies published to date are conflicting. A review identified six trials, only two of which were double-blind , placebo -controlled, randomized controlled trials , that could be used to evaluate the effect of vitamin C supplementation on the prevention or treatment of pneumonia Overall, vitamin C supplementation had a mild beneficial effect compared to placebo.
However, methodological shortcomings and the highly variable characteristics of the study populations prevent comparisons and firm conclusions from the available data. At this time, prophylactic use of vitamin C supplements for pneumonia prevention and treatment cannot be advocated for the general population.
For a review of vitamin C and the common cold, see the article on Vitamin C. Vitamin E is a lipid -soluble antioxidant that protects the integrity of cell membranes from damage caused by free radicals In particular, the α-tocopherol form of vitamin E protects against peroxidation of polyunsaturated fatty acids , which can potentially cause cellular damage and subsequently lead to improper immune responses Several studies in animal models, as well as humans, indicate that vitamin E deficiency impairs both humoral and cell-mediated aspects of adaptive immunity, including B and T cell function reviewed in Moreover, vitamin E supplementation in excess of current intake recommendations has been shown to enhance immunity and decrease susceptibility to certain infections, especially in elderly individuals.
The natural age-related decline of the immune function is accompanied by an increased susceptibility to infections, a poorer response to immunization, and higher risks of developing cancers and autoimmune diseases. α-Tocopherol has been shown to enhance specifically the T cell-mediated immune response that declines with advancing age reviewed in T cell impaired response has been partly associated with a reduced capacity of naïve T cells to be activated during antigen presentation, and to produce interleukin-2 IL-2 and proliferate as a result However, very few studies have addressed the potential association between α-tocopherol and immune function in humans Lower α-tocopherol doses failed to improve the DTH response compared to a placebo in another study in healthy participants ages, years Yet, other trials have not reported an overall beneficial effect of vitamin E supplements on respiratory tract infections in older adults , More research is needed to examine whether supplemental vitamin E might enhance immune function and reduce risk of infection in older adults.
Vitamin B 6 is required in the endogenous synthesis and metabolism of amino acids — the building blocks of proteins like cytokines and antibodies. Animal and human studies have demonstrated that vitamin B 6 deficiency impairs aspects of adaptive immunity, including both humoral and cell-mediated immunity.
Specifically, deficiency in this micronutrient has been shown to affect lymphocyte proliferation , differentiation , and maturation as well as cytokine and antibody production Correcting the vitamin deficiency restores the affected immune functions This pathway is known to be activated during pro- inflammatory immune responses and plays a critical role in immune tolerance of the fetus during pregnancy Key intermediates in the tryptophan-kynurenine pathway are involved in the regulation of immune responses.
Several tryptophan derivatives have been found to induce the death apoptosis or block the proliferation of certain types of immune cells, such as lymphocytes in particular T-helper 1. They can also inhibit the production of pro-inflammatory cytokines reviewed in There is evidence to suggest that adequate vitamin B 6 intake is important for optimal immune system function, especially in older individuals , Furthermore, chronic inflammation that triggers tryptophan degradation and underlies many diseases e.
The B vitamin, folate , is required as a coenzyme to mediate the transfer of one-carbon units. Folate coenzymes act as acceptors and donors of one-carbon units in a variety of reactions critical to the endogenous synthesis and metabolism of nucleic acids DNA and RNA and amino acids , Thus, folate has obvious importance in immunity.
Animal studies and a few observational studies in humans indicate that folate deficiency is associated with an increased susceptibility to infection Clinical folate deficiency, known as megaloblastic anemia , results in impaired immune responses, primarily affecting cell-mediated immunity; correcting the vitamin deficiency with folic acid supplementation restores the affected immune functions Animal studies indicate that antibody responses of humoral immunity may also be impaired in folate deficiency, though human studies in this regard are lacking In humans, vitamin B 12 functions as a coenzyme for two enzymatic reactions.
One of the vitamin B 12 -dependent enzymes is involved in the synthesis of the amino acid , methionine , from homocysteine. Methionine in turn is required for the synthesis of S-adenosylmethionine, a methyl group donor used in many biological methylation reactions, including the methylation of a number of sites within DNA and RNA.
The other vitamin B 12 -dependent enzyme, L-methylmalonyl-CoA mutase, converts L-methylmalonyl-CoA to succinyl-CoA, a compound that is important in the production of energy from fats and proteins , as well as in the synthesis of hemoglobin — the oxygen carrying pigment in red blood cells Patients with diagnosed vitamin B 12 deficiency as pernicious anemia or megaloblastic anemia have been reported to have suppressed natural killer cell activity and decreased numbers of circulating lymphocytes , One study found that these immunomodulatory effects were corrected by treating the vitamin deficiency Zinc is critical for normal development and function of cells that mediate both innate and adaptive immunity The cellular functions of zinc can be divided into three categories: 1 catalytic, 2 structural, and 3 regulatory see the article on Zinc Because zinc is not stored in the body, regular dietary intake of the mineral is important in maintaining the integrity of the immune system.
Thus, inadequate intake can lead to zinc deficiency and compromised immune responses With respect to innate immunity, zinc deficiency impairs the complement system, cytotoxicity of natural killer cells , phagocytic activity of neutrophils and macrophages , and immune cell ability to generate oxidants that kill invading pathogens Zinc deficiency also compromises adaptive immune function, including lymphocyte number and function T lymphocytes T cells are particularly vulnerable to zinc deficiency reviewed in Zinc deficiency causes thymic atrophy , which leads to low numbers of T cells, and creates an imbalance in T helper cell subsets, with a shift towards Th2.
Additionally, altered cytokine production during zinc deficiency can contribute to oxidative stress and inflammation , ; reviewed in Even marginal zinc deficiency, which is more common than severe zinc deficiency, can suppress aspects of immunity The elderly may be particularly at risk for marginal zinc deficiency given that there is a high prevalence of inadequate dietary zinc intake among those 60 years of age and older , and that plasma zinc concentration declines with age , It is not known why plasma zinc declines, but impaired absorption, alterations in cellular uptake, and epigenetic dysregulation may be contributing factors reviewed in For more information on zinc supplementation and the susceptibility to infectious diseases, such as diarrhea, pneumonia, and malaria, see the article on Zinc.
Adequate selenium intake is essential for the host to mount a proper immune response because it is required for the function of several selenium-dependent enzymes known as selenoproteins see the article on Selenium.
For example, the glutathione peroxidases GPx are selenoproteins that function as important redox regulators and cellular antioxidants , which reduce potentially damaging reactive oxygen species , such as hydrogen peroxide and lipid hydroperoxides, to harmless products like water and alcohols by coupling their reduction with the oxidation of glutathione see Figure 2 in the article on selenium These roles have implications for immune function and cancer prevention.
Selenium deficiency impairs aspects of innate and adaptive immunity , , adversely affecting both humoral immunity i. Selenium deficiency also appears to enhance the virulence or progression of some viral infections see the article on Selenium Selenium affects different types of immune responses in different ways, and the selenium status of the host is an important factor when considering selenium supplementation For example, selenium supplementation improves cell-mediated immunity in deficient individuals and enhances the immune response to viruses; on the other hand, selenium supplementation may worsen allergic asthma and impair the immune response to parasites , A considerable amount of basic research also indicates that selenium plays a role in regulating the production of cytokines and eicosanoids that orchestrate the immune response , Iron is an essential component of hundreds of proteins and enzymes that are involved in oxygen transport and storage, electron transport and energy generation, antioxidant and beneficial pro-oxidant functions, and DNA synthesis see the article on Iron Iron is required by the host in order to mount effective immune responses to invading pathogens , and iron deficiency impairs immune responses Sufficient iron is critical to several immune functions, including the differentiation and proliferation of T lymphocytes and generation of reactive oxygen species ROS that kill pathogens.
However, iron is also required by most infectious agents for replication and survival. During an acute inflammatory response, serum iron levels decrease while levels of ferritin the iron storage protein increase, suggesting that sequestering iron from pathogens is an important host response to infection , , Moreover, conditions of iron overload e.
Concern that iron administration could increase susceptibility to malaria and the risk of adverse events has received a lot of well-deserved attention A large, randomized controlled trial RCT in Pemba, Zanzibar, where malaria is endemic, reported an increase in serious adverse events hospital admissions and deaths among young children ages, months receiving iron plus folic acid supplements compared to those receiving placebo [ RR : 1.
A Cochrane review found that oral iron supplementation alone did not influence the risk of clinical malaria fever plus parasitemia 13 trials , death 13 trials , or hospital admissions 4 trials in malaria-endemic areas However, a subgroup analysis revealed that the risk for clinical malaria was higher with iron supplementation in settings that lacked malaria surveillance and treatment [RR: 1.
With respect to other infections, the Cochrane review found no beneficial or adverse effects of iron supplementation on respiratory tract infections 11 RCTs or diarrheal episodes 13 RCTs Copper is a critical functional component of a number of essential enzymes known as cuproenzymes see the article on Copper.
The mineral plays an important role in the development and maintenance of immune system function, but the exact mechanism of its action is not yet known. Copper has antimicrobial properties, accumulates at sites of inflammation , and may play a role in the innate immune response to bacterial infections reviewed in Adverse effects of insufficient copper on immune function appear most pronounced in infants.
Infants with Menkes disease, a genetic disorder that results in severe copper deficiency, suffer from frequent and severe infections , In a study of 11 malnourished infants with evidence of copper deficiency, the ability of certain white blood cells to engulf pathogens increased significantly after one month of copper supplementation Immune effects have also been observed in adults with low intake of dietary copper.
In one study, 11 men on a low-copper diet 0. While it is known that severe copper deficiency has adverse effects on immune function, the effects of marginal copper deficiency in humans are not yet clear However, long-term high intakes of copper can result in adverse effects on immune function.
In a small feeding study conducted in nine healthy young men, long-term high intake of copper 7. Probiotics are usually defined as live microorganisms that, when administered in sufficient amounts, benefit the overall health of the host Common examples belong to the Lactobacilli and Bifidobacteria species; these probiotics are consumed in yogurt and other fermented foods.
Ingested probiotics that survive digestion can transiently inhabit the lower part of the gastrointestinal tract Here, they can modulate immune functions by interacting with various receptors on intestinal epithelial cells and other gut-associated immune cells, including dendritic cells and M-cells Immune modulation requires regular consumption because probiotics have not been shown to permanently alter intestinal microflora Probiotics have been shown to benefit both innate and adaptive immune responses of the host Proposed mechanisms by which probiotics may influence immunity include the maintenance of the antimicrobial barrier, production of metabolic products that inhibit the growth of pathogens and influence host immune cell activity, and competition with pathogenic bacteria for available resources 13 , For example, probiotics can strengthen the gut epithelial barrier — an important innate defense — through a number of ways, such as by inhibiting apoptosis and promoting the survival of intestinal epithelial cells Probiotics can also stimulate the production of antibodies and T lymphocytes , which are critical in the adaptive immune response Several immune effects of probiotics are mediated through altering cell-signaling cascades that modify cytokine and other protein expression However, probiotics exert diverse effects on the immune system that are dependent not only on the specific strain but also on the dose, route, and frequency of delivery Specifically, the incidence of CDAD in the probiotic group was 2.
This effect applied to both children and adults and was evident regardless of the dose or strain of administered probiotic. Another systematic review and meta-analysis , which focused on hospitalized adults ages 33 to 79 years , reported a significant reduction in antibiotic-associated diarrhea RR : 0.
At this time, the scientific evidence is too weak to advocate the use of probiotics to reduce respiratory infections and improve vaccination response, especially in the elderly reviewed in , Probiotics may have utility in the prevention of inflammatory bowel disorders, allergic diseases, gastrointestinal and other types of infections, and certain cancers , but the clinical efficacy of probiotic administration for these applications is unknown at this time Overnutrition can create an imbalance between energy intake and energy expenditure and lead to excessive energy storage, resulting in obesity Obesity is a major public health problem worldwide, especially in industrialized nations.
Obese individuals are at increased risk of morbidity from a number of chronic diseases , including hypertension and cardiovascular disease , type 2 diabetes mellitus , liver and gallbladder disease, osteoarthritis, sleep apnea , and certain cancers Obesity has also been linked to increased risk of mortality Overnutrition and obesity have been shown to alter immunocompetence.
Obesity is associated with macrophage infiltration of adipose tissue ; macrophage accumulation in adipose tissue is directly proportional to the degree of obesity Studies in mouse models of genetic and high-fat diet-induced obesity have documented a marked upregulation in expression of inflammation and macrophage-specific genes in white adipose tissue In fact, obesity is characterized by chronic, low-grade inflammation, and inflammation is thought to be an important contributor in the pathogenesis of insulin resistance — a condition that is strongly linked to obesity.
A number of changes occur in hypertrophied adipose tissue that might contribute to this inflammatory state: 1 altered adipokine secretion, namely increased leptin pro-inflammatory and reduced adiponectin anti-inflammatory secretion; 2 release of free fatty acids that induce systemic inflammation; 3 increased endoplasmic reticulum stress leading to oxidative stress and inflammation triggered by adipocyte expansion; and 4 increased inflammatory gene expression and immune cell activation in hypoxic regions Alterations in the numbers, proportions, and activity of resident adipose tissue immune cells also help explain the pro-inflammatory phenotype of obesity , Notably, visceral fat accumulation central adiposity appears to be more strongly associated with inflammation and adverse metabolic risk factors than subcutaneous fat, displaying increased macrophage infiltration, lower adiponectin gene expression, and increased inflammatory gene expression , Adipose tissue secretes fatty acids and other molecules, including various hormones and cytokines called adipocytokines or adipokines , that trigger inflammatory processes Leptin is one such hormone and adipokine that plays a key role in the regulation of food intake, body weight, and energy homeostasis , Leptin is secreted from adipose tissue and circulates in direct proportion to the amount of fat stores.
Normally, higher levels of circulating leptin suppress appetite and thereby lead to a reduction in food intake Obese individuals have been reported to have higher plasma leptin concentrations compared to lean individuals. However, in the obese, the elevated leptin signal is not associated with the normal responses of reduced food intake and increased energy expenditure, suggesting obesity is associated with a state of leptin resistance.
Leptin resistance has been documented in mouse models of obesity, but more research is needed to better understand leptin resistance in human obesity Leptin has a number of other functions as well, such as modulation of inflammatory responses and aspects of humoral and cell-mediated responses of the adaptive immune system , Specific effects of leptin, elucidated in animal and in vitro studies, include the promotion of phagocytic function of immune cells; stimulation of pro-inflammatory cytokine production; and regulation of neutrophil , natural killer NK cell , and dendritic cell functions reviewed in Leptin also affects aspects of cell-mediated immunity; for example, leptin promotes T helper Th 1 immune responses and thus may have implications in the development of autoimmune disease Th1 cells are primarily involved in activating macrophages and inflammatory responses 4 , Obese individuals may exhibit increased susceptibility to various infections.
Some epidemiological studies have shown that obese patients have a higher incidence of postoperative and other nosocomial infections compared with patients of normal weight , ; reviewed in Obesity has been linked to poor wound healing and increased occurrence of skin infections A higher body mass index BMI may also be associated with increased susceptibility to respiratory, gastrointestinal , liver, and biliary infections reviewed in Several epidemiological studies have reported obesity to be an independent risk factor for increased morbidity and mortality following infection with the influenza A H1N1 virus In obesity, the increased vulnerability, severity, or complications of certain infections may be related to a number of factors, such as select micronutrient deficiencies.
For example, one study in obese children and adolescents associated impairments in cell-mediated immunity with deficiencies in zinc and iron Deficiencies or inadequacies of other vitamins, including the B vitamins and vitamins A, C, D, and E, have also been associated with obesity Overall, immune responses appear to be compromised in obesity, but more research is needed to clarify the relationship between obesity and infection-related morbidity and mortality reviewed in Written in August by: Victoria J.
Drake, Ph. Linus Pauling Institute Oregon State University. Updated in October by: Giana Angelo, Ph. Reviewed in July by: Adrian F. Gombart, Ph. Associate Professor Department of Biochemistry and Biophysics Principal Investigator, Linus Pauling Institute Oregon State University. The update of this article was underwritten, in part, by a grant from Bayer Consumer Care AG , Basel, Switzerland.
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