Effect of Vitamin D Deficiency and Supplementation in Lactation and Early Life on Allergic Airway Inflammation and the Expression of Autophagy-Related Genes in an Ovalbumin Mouse Model

Early-life vitamin D deficiency is associated with adverse child health outcomes, but the prevalence of vitamin D deficiency and its correlates in infants remains underexplored, particularly in sub-Saharan Africa. We aimed to investigate the prevalence of vitamin D deficiency and its correlates among young infants in South Africa. This study included 744 infants, aged 6–10 weeks from the Drakenstein Child Health Study, a population-based birth cohort. Infants were categorized into distinct categories based on serum 25(OH)D concentration level including deficient (<50 nmol/L), insufficient (50–74 nmol/L), and sufficient (≥75 nmol/L). Using multivariable Tobit and logistic regression models, we examined the correlates of serum 25(OH)D3 levels. The overall prevalence of vitamin D deficiency was 81% (95% confidence intervals (CI]) 78–83). Multivariable regression analysis showed that serum 25(OH)D3 concentration was independently associated with study site, socioeconomic status, and sex. Birth in winter and breastfeeding were the strongest predictors of lower serum 25(OH)D3 concentration levels. Compared to non-breastfed children, children breastfed were at higher risk of vitamin D deficiency (AOR, 1.96; 95% CI, 1.04–3.67) and breastfeeding for more than one month was associated with greater likelihood of vitamin D deficiency (AOR, 5.40; 95% CI, 2.37–12.32) and lower vitamin D concentrations (−16.22 nmol/L; 95% CI, −21.06, −11.39). Vitamin D deficiency in infants is ubiquitous, under-recognised, and strongly associated with season of birth and breastfeeding in this setting. Nutritional interventions with vitamin D supplementation in national health programs in low- and middle-income countries are urgently needed to improve early-life vitamin D status in infants.

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Early-life persistent vitamin D deficiency-induced cardiovascular dysfunction in mice is mediated by transient receptor potential C channels

The Journal of Steroid Biochemistry and Molecular Biology ◽

10.1016/j.jsbmb.2020.105804 ◽

2021 ◽

Vol 206 ◽

pp. 105804

Author(s):

Kimberly Stratford ◽

Najwa Haykal-Coates ◽

Leslie Thompson ◽

Aimen Farraj ◽

Mehdi Hazari

Keyword(s):

Vitamin D ◽

Vitamin D Deficiency ◽

Early Life ◽

Transient Receptor Potential ◽

Receptor Potential ◽

Cardiovascular Dysfunction ◽

Transient Receptor

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OVA-Induced Allergic Airway Inflammation Mouse Model

Methods in Molecular Biology - Pre-Clinical Models ◽

10.1007/978-1-4939-8994-2_28 ◽

2018 ◽

pp. 297-301 ◽

Cited By ~ 5

Author(s):

Mateus Casaro ◽

Vanessa R. Souza ◽

Fernando A. Oliveira ◽

Caroline M. Ferreira

Keyword(s):

Mouse Model ◽

Airway Inflammation ◽

Allergic Airway Inflammation

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Allergen-Specific Treg Cells Upregulated by Lung-Stage S. japonicum Infection Alleviates Allergic Airway Inflammation

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2021.678377 ◽

2021 ◽

Vol 9 ◽

Author(s):

Zhidan Li ◽

Wei Zhang ◽

Fang Luo ◽

Jian Li ◽

Wenbin Yang ◽

...

Keyword(s):

Mouse Model ◽

Protective Effect ◽

Airway Inflammation ◽

Lung Tissue ◽

Immunoglobulin E ◽

Allergic Airway Inflammation ◽

Treg Cells ◽

Protective Effects ◽

Novel Therapy ◽

Allergen Sensitization

Schistosoma japonicum infection showed protective effects against allergic airway inflammation (AAI). However, controversial findings exist especially regarding the timing of the helminth infection and the underlying mechanisms. Most previous studies focused on understanding the preventive effect of S. japonicum infection on asthma (infection before allergen sensitization), whereas the protective effects of S. japonicum infection (allergen sensitization before infection) on asthma were rarely investigated. In this study, we investigated the protective effects of S. japonicum infection on AAI using a mouse model of OVA-induced asthma. To explore how the timing of S. japonicum infection influences its protective effect, the mice were percutaneously infected with cercaria of S. japonicum at either 1 day (infection at lung-stage during AAI) or 14 days before ovalbumin (OVA) challenge (infection at post–lung-stage during AAI). We found that lung-stage S. japonicum infection significantly ameliorated OVA-induced AAI, whereas post–lung-stage infection did not. Mechanistically, lung-stage S. japonicum infection significantly upregulated the frequency of regulatory T cells (Treg cells), especially OVA-specific Treg cells, in lung tissue, which negatively correlated with the level of OVA-specific immunoglobulin E (IgE). Depletion of Treg cells in vivo partially counteracted the protective effect of lung-stage S. japonicum infection on asthma. Furthermore, transcriptomic analysis of lung tissue showed that lung-stage S. japonicum infection during AAI shaped the microenvironment to favor Treg induction. In conclusion, our data showed that lung-stage S. japonicum infection could relieve OVA-induced asthma in a mouse model. The protective effect was mediated by the upregulated OVA-specific Treg cells, which suppressed IgE production. Our results may facilitate the discovery of a novel therapy for AAI.

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Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish

Scientific Reports ◽

10.1038/s41598-020-72622-2 ◽

2020 ◽

Vol 10 (1) ◽

Cited By ~ 1

Author(s):

Megan M. Knuth ◽

Debabrata Mahapatra ◽

Dereje Jima ◽

Debin Wan ◽

Bruce D. Hammock ◽

...

Keyword(s):

Vitamin D ◽

Vitamin D Deficiency ◽

Early Life ◽

Life Stage ◽

Somatic Growth ◽

Early Life Stage ◽

Cytokine Signaling ◽

Central Adiposity ◽

Stage Development ◽

Life Stage Development

Abstract Emerging evidence demonstrates the importance of sufficient vitamin D (1α, 25-dihydroxyvitamin D3) levels during early life stage development with deficiencies associated with long-term effects into adulthood. While vitamin D has traditionally been associated with mineral ion homeostasis, accumulating evidence suggests non-calcemic roles for vitamin D including metabolic homeostasis. In this study, we examined the hypothesis that vitamin D deficiency (VDD) during early life stage development precedes metabolic disruption. Three dietary cohorts of zebrafish were placed on engineered diets including a standard laboratory control diet, a vitamin D null diet, and a vitamin D enriched diet. Zebrafish grown on a vitamin D null diet between 2–12 months post fertilization (mpf) exhibited diminished somatic growth and enhanced central adiposity associated with accumulation and enlargement of visceral and subcutaneous adipose depots indicative of both adipocyte hypertrophy and hyperplasia. VDD zebrafish exhibited elevated hepatic triglycerides, attenuated plasma free fatty acids and attenuated lipoprotein lipase activity consistent with hallmarks of dyslipidemia. VDD induced dysregulation of gene networks associated with growth hormone and insulin signaling, including induction of suppressor of cytokine signaling. These findings indicate that early developmental VDD impacts metabolic health by disrupting the balance between somatic growth and adipose accumulation.

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