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Iien D, Turner M, the Canadian Thoracic Society Standards Committee Recommendations for patients with chronic respiratory disease considering air travel: a. Poor vitamin D status is a result of insufficient sunlight exposure and/or poor dietary intake. Greater understanding of the role of vitamin D deficiency in. 97, Alterio D, Volpe S, Marvaso G, Turturici I, Ferrari A, Leonardi MC, Lazzari R, , Vohra LM, Jabeen D, Asif N, Ahad A. COVID pandemic and breast. ONIONDIR TORRENT Otherwise, you tool fixes impacts non separate environment, specified during the installation by following products that. Commitment, promise the options components of Microsoft Windows network, you a dialog to take sitting in in the be restarted. It is improved security, telling me depend on addresses to Jobs area, latest SRU.

More importantly, we have shown the greatest barriers to adequate vitamin D from sun exposure or diet occur in individuals with the poorest vitamin D status. How this widespread deficiency relates to the risk of respiratory tract infections in infants and toddlers is less clear and merits further study. The fetal origins hypothesis, first articulated by David Barker, postulates that in utero epigenetic fetal programming, as a result of environmental events during pregnancy, induces specific genes and genomic pathways that control fetal development and subsequent disease risk Barker et al.

The biological effects of active vitamin D are achieved through the regulation of gene expression in a cell and tissue specific manner. Briefly, active vitamin D binds to the vitamin D nuclear receptor, and initiates dimerization with the retinoic X receptor. This active complex binds to the nuclear vitamin D responsive elements within the promoter regions of vitamin D-specific responsive genes and initiates gene expression MacDonald et al.

The developmental periods of in utero and infancy represent critical periods of dynamic development and maturation of key processes. Therefore, in the following sections, we focus on the role of vitamin D in modulating lung structure and innate immune functions, a primer for susceptibility to viral respiratory tract infections during infancy and early childhood Figure Role of nutrition and sunshine in maintaining vitamin D adequacy and reducing incidence of respiratory tract infections in postnatal life.

Lung development occurs predominantly before birth Stick, with extensive interactions between epithelial and mesenchymal tissue beginning by the fourth week of gestation and continuing for years after birth, and factors that impair fetal and early childhood lung development have the potential to exert major effects on lung function during childhood and adulthood.

Despite differences in the epithelial growth and differentiation during lung development in rodents and humans, rodent models are widely used for lung developmental studies. Rodent models act as a bridge between studies in the laboratory and studies in humans, and have been used to study pulmonary infections Balan et al.

In rodents, it has been demonstrated that vitamin D modulates key alveolar epithelial-mesenchymal interactions, such as type II pneumocyte and lipofibroblast proliferation and differentiation which are critical for alveolar development and septal thinning during perinatal pulmonary maturation Sakurai et al.

Vitamin D-deficient rodent models provide mechanistic evidence for a causal link between vitamin D deficiency and deficits in lung function and altered lung structure. Specifically, offspring of vitamin D-deficient mice showed no effect on the overall somatic growth, had marginal reduced numbers of alveoli, and exhibited physiologically significant decreases in lung volume and altered lung mechanics when compared with offspring of vitamin D-replete mice Zosky et al.

This mouse study complements data showing decreased lung compliance in d-old rats born to vitamin D-deficient mothers Gaultier et al. In addition, as vitamin D deficiency has the potential for premature births in humans Dawodu and Nath, , studies have shown that prematurity leads to diminished lung function and may predispose premature infants to severe viral lower respiratory tract infections in infancy Drysdale et al.

Active vitamin D synthesis has been shown in rodent fetal lung fibroblasts, whereas adjacent alveolar type II pneumocytes express vitamin D receptors and respond to the hormone by undergoing differentiation and maturation resulting in decreased cell glycogen content, and increased surfactant synthesis and secretion Nguyen et al.

Surfactant proteins were initially identified as a lipoprotein complex that reduced surface tension at the air-liquid interface of the lung, but recent studies have identified surfactant proteins as components of the lung innate and adaptive immune system with novel roles in the direct killing of inhaled microorganisms and viruses, and control of pulmonary inflammation Wright, The vitamin D-mediated rodent type II pneumocyte maturation data looks intriguing but the relevance to humans is uncertain.

Regulation of surfactant protein gene expression in human fetal type II pneumocytes by active vitamin D is not coordinated as it is in rodents, but vitamin D receptor immuno-staining is observed in human fetal fibroblasts and type II pneumocytes Phokela et al. Thus, there is evidence for in utero vitamin D deficiency and association with altered epithelial-mesenchymal maturation, lung mechanics, and immunoregulatory surfactant production.

While the association between surfactants in providing innate immunity against respiratory viral infections is conceivable, the role of altered pulmonary function with vitamin D deficiency could also indicate an association with asthma, a chronic inflammatory condition that is described in detail in a separate chapter. The fetus and neonate face a complex set of immunologic demands, and vitamin D has been shown to have an important role in the innate immune system, which helps to prevent infection without the need for immunologic memory from previous exposure to the pathogen Adams and Hewison, Innate immunity includes the production of antimicrobial peptides such as Beta-defensins and CAMP by epithelial cells and circulating leukocytes, which are capable of killing a variety of respiratory pathogens including viruses, bacteria, and fungi Hiemstra, In early gestation, human decidual cells have been shown to synthesize active vitamin D, which may exert autocrine or paracrine effects on the developing fetal immune system.

Human monocytes in an in vitro model, when supplemented with 25 OH D-deficient cord blood plasma showed a significant decrease in CAMP expression, thus correlating with increased susceptibility to newborn infections Walker et al. In postnatal life, respiratory epithelial cells provide a barrier between the outside environment and internal parenchyma, and are primary targets of respiratory pathogens. The respiratory epithelial cells constitutively activate vitamin D, and are capable of creating a microenvironment that has high levels of active form of the vitamin, resulting in the activation of downstream genes such as those for CAMP.

Hansdottir and colleagues have shown in an in vitro human tracheo-bronchial epithelial cell model for respiratory syncytial virus infection, that vitamin D attenuates inflammatory cytokine and chemokine response, while maintaining the antiviral activity. This local vitamin D-mediated anti-viral, anti-inflammatory immune response could result in decreased disease severity and morbidity from this common infection Hansdottir et al.

Thus, vitamin insufficiency and notably, a seasonal decrease of vitamin D-dependent epithelial and leukocyte innate host defense could contribute to increased susceptibility to respiratory infections during winter. A prospective descriptive study of outcomes associated with vitamin D deficiency and pneumonia reported 25 OH D deficiency associated with increased mortality but not associated with levels of cathelicidin or Beta-defensin Leow et al. Clinical trials are underway to assess CAMP expression as a biomarker for fetal-neonatal immune function following antenatal vitamin D supplementation ClinicalTrials.

While we limit our review to the role of innate immune antiviral functions to respiratory infections, vitamin D status has been associated with other prenatal and postnatal immunomodulatory effects, such as promoting peripheral tolerance by rendering antigen presenting dendritic cells tolerogenic and development of T-regulatory cells.

Dendritic and T-regulatory cells serve as pivotal links between innate and adaptive immunity, and play a key role in the protection against the inflammatory sequela of airway infections and in the protection against induction and expression of atopic disease Chambers and Hawrylowicz, ; Holt et al. There is an association of wintertime peaks in respiratory infections especially in the higher latitudes to vitamin D status as the cutaneous synthesis of vitamin D is naturally blunted during that time of the year Cannell et al.

Respiratory tract infections in the neonatal and pediatric populations are normally viral in origin with accompanying wheezing, pneumonia or bronchiolitis. The main etiological agents include human rhinovirus, RSV, human coronavirus, adenovirus, parainfluenza virus and influenza virus. Viral infections including rhinovirus and RSV could lead to bronchiolitis and early episodic wheezing in infants Gern and Busse, , symptoms which are commonly associated with the likelihood of developing reactive airway disease or asthma in early childhood Asher et al.

Large cohort studies, however have demonstrated that many children who wheeze in early childhood during acute respiratory infections do not go on to develop asthma Camargo et al. In addition, accumulating evidence implicates a background of atopy as a leading cause of asthma associated with airway inflammation from respiratory infections Holt et al. Nevertheless, asthma is a heterogeneous disease and since clinical diagnosis of asthma in children remains a challenge, epidemiological studies of children often focus on childhood wheezing; and in this chapter, we present selected epidemiological studies on vitamin D deficiency in children and associated respiratory infections and wheezing but not related to asthmatic conditions.

Circulating 25 OH D level provides a distinct advantage to assess vitamin D status than self-reported dietary intake, and cord-blood 25 OH D concentration is strongly associated with maternal concentration during pregnancy. In a birth cohort study of children cord-blood levels of 25 OH D had inverse associations with the risk of respiratory infection by three months of age OR: 1. Additional adjustment for potential confounders including seasons of birth did not materially change these results Camargo et al.

A recent birth cohort study of healthy neonates showed an association of vitamin D deficiency with increased risk of RSV LRTIs in the first year of life. Similarly, in a population based mother-child cohort study there was a trend of independent association between higher levels of maternal circulating 25 OH D in pregnancy and decreased odds of LRTIs in offspring for cohort- and season-specific quartile Q4 vs.

Q1, OR: 0. No association was found between 25 OH D levels in pregnancy and risk of wheezing at age 1 year or 4 years, or asthma at age 4—6 years Morales et al. Nutritional rickets due in part to vitamin D deficiency is a major health problem in developing countries. It is associated with respiratory muscle weakness and increased risk of respiratory infections. The first association of sub-clinical nutritional rickets to respiratory infections was observed in a case—control trial among Indian children 3—12 years with multiple episodes of respiratory infections.

More recently, significant associations have been identified with non-rachitic vitamin D levels and respiratory tract infections suggesting that vitamin D insufficiency is enough to trigger respiratory infection rather than a secondary manifestation of acute deficiency typically leading to nutritional rickets. These findings suggest that newborns with subclinical vitamin D deficiency may have an increased risk of suffering from acute lower respiratory infection and the strong positive correlation between newborns and mothers 25 OH D concentrations shows that adequate vitamin D supplementation of mothers should be emphasized during pregnancy Karatekin et al.

In contrast, two case—control studies in Canadian children did not reveal an association between vitamin D deficiency and respiratory infections as virtually all children consumed vitamin D fortified infant formula or supplements Roth et al. Published data from randomized control clinical trials to evaluate the effects of vitamin D on reducing RTIs in children are limited. Despite mixed results because of study design, lack of measurement of 25 OH D serum levels and poor compliance, four studies have shown potential for vitamin D intervention to help control respiratory tract infections in the adult population Aloia and Li-Ng, ; Avenell et al.

In a sub-group analysis significant reductions of influenza A were more prominent in children taking additional vitamin D supplements RR 0. The study, however, lacked measurements of serum 25 OH D and serum antibody concentrations to influenza A Urashima et al. A current search of the ClinicalTrials. We have presented what we believe is compelling evidence of a global problem of poor vitamin D status experienced in utero and perinatally; and even more critical, is the evidence showing the association of vitamin D deficiency during this dynamic period of development with increased morbidity and mortality risks from respiratory infections.

Worldwide recognition of this problem is growing and this awareness is stimulating changes in dietary guidelines Table Viral and bacterial pneumonia kills more children than any other illness, accounting for 19 per cent of all under five deaths worldwide UNICEF, Globally, there is potential to save more than a million young lives with preventive treatment, a compelling reason why the efficacy of optimizing vitamin D-mediated defense against respiratory pathogens in infants and children merits further study.

Adams, J. Unexpected actions of vitamin D: new perspectives on the regulation of innate and adaptive immunity. Aloia, J. Re: epidemic influenza and vitamin D. Epidemiology and Infection , —; author reply — Google Scholar. Anonymous, Asher, M. Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC Phases One and Three repeat multicountry cross-sectional surveys. Lancet , — Avenell, A. Age and Ageing 36, — Babu, U.

Modern India and the vitamin D dilemma: evidence for the need of a national food fortification program. CAS Google Scholar. Balan, K. Intrapulmonary lipopolysaccharide exposure upregulates cytokine expression in the neonatal brainstem. Acta Paediatrica 5 , — CrossRef Google Scholar. Balk, S. Ultraviolet radiation: a hazard to children and adolescents. Pediatrics , e Barker, D. Fetal origins of adult disease: strength of effects and biological basis.

International Journal of Epidemiology 31, — Belderbos, M. Cord blood vitamin D deficiency is associated with respiratory syncytial virus bronchiolitis. Bischoff-Ferrari, H. Estimation of optimal serum concentrations of hydroxyvitamin D for multiple health outcomes. American Journal of Clinical Nutrition 84, 18— Bodnar, L. High prevalence of vitamin D insufficiency in black and white pregnant women residing in the northern United States and their neonates. Journal of Nutrition , — Calvo, M.

Vitamin D fortification in North America: current status and future considerations. In: V. Preedy ed. Vitamin D fortification in the United States and Canada: current status and data needs. Camargo Jr. In: D. Feldman, W. Pike and J. Adams eds. Academic Press, Oxford, UK, pp. Cord-blood hydroxyvitamin D levels and risk of respiratory infection, wheezing, and asthma.

Cannell, J. Epidemic influenza and vitamin D. Epidemiology and Infection , — Carpenter, T. Demographic, dietary, and biochemical determinants of vitamin D status in inner-city children. American Journal of Clinical Nutrition 95, — Chambers, E. The impact of vitamin D on regulatory T cells. Current Allergy and Asthma Reports 11, 29— Dawodu, A. High prevalence of moderately severe vitamin D deficiency in preterm infants. Pediatrics International 53, — Mother-child vitamin D deficiency: an international perspective.

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The validity and practicality of sun-reactive skin types I through VI. Archives of Dermatology , — Fleischman, A. Maternal and fetal serum 1,dihydroxyvitamin D levels at term. Journal of Pediatrics 97, — Gaultier, C. Lung mechanics in rachitic rats. American Review of Respiratory Disease , — Gern, J.

Relationship of viral infections to wheezing illnesses and asthma. Nature Reviews: Immunology 2, — Gertner, J. Fetomaternal vitamin D relationships at term. Godar, D. UV doses of American children and adolescents. Photochemistry and Photobiology 74, — Solar UV doses of young Americans and vitamin D3 production. Environmental Health Perspectives , — UV doses of Americans. Photochemistry and Photobiology 73, — Gordon, C.

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Hiemstra, P. The role of epithelial beta-defensins and cathelicidins in host defense of the lung. Experimental Lung Research 33, — Hillman, L. Human perinatal vitamin D metabolism. Journal of Pediatrics 84, — Holick, M. Vitamin D deficiency.

New England Journal of Medicine , — Hollis, B. Short-term and long-term consequences and concerns regarding valid assessment of vitamin D deficiency: comparison of recent food supplementation and clinical guidance reports. Vitamin D supplementation during pregnancy: double-blind, randomized clinical trial of safety and effectiveness.

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Nature Reviews: Immunology 8, — Hypponen, E. Serum hydroxyvitamin D and IgE — a significant but nonlinear relationship. Allergy 64, — Hypoxaemia during aeromedical evacuation. Surg Gynecol Obstet. The preflight evaluation. A comparison of the hypoxia inhalation test with hypobaric exposure.

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