Maternal Vitamin D Level Is Associated with Viral Toll-Like Receptor Triggered IL-10 Response but Not the Risk of Infectious Diseases in Infancy

Abstract

Reports on the effect of prenatal vitamin D status on fetal immune development and infectious diseases in childhood are limited. The aim of this study was to investigate the role of maternal and cord blood vitamin D level in TLR-related innate immunity and its effect on infectious outcome. Maternal and cord blood 25 (OH)D level were examined from 372 maternal-neonatal pairs and their correlation with TLR-triggered TNF-α, IL-6, and IL-10 response at birth was assessed. Clinical outcomes related to infection at 12 months of age were also evaluated. The result showed that 75% of the pregnant mothers and 75.8% of the neonates were vitamin deficient. There was a high correlation between maternal and cord 25(OH)D levels (r = 0.67, p < 0.001). Maternal vitamin D level was inversely correlated with IL-10 response to TLR3 (p = 0.004) and TLR7-8 stimulation (p = 0.006). However, none of the TLR-triggered cytokine productions were associated with cord 25(OH)D concentration. There was no relationship between maternal and cord blood vitamin D status with infectious diseases during infancy. In conclusion, our study had shown that maternal vitamin D, but not cord vitamin D level, was associated with viral TLR-triggered IL-10 response.

Low cord-serum 25-hydroxyvitamin D levels are associated with poor lung function performance and increased respiratory infection in infancy

“…In this study, the mean 25(OH)D level in the cord serum (13.8 ng/mL) was comparable with other reports, but a lower mean level in the maternal serum (15.0 ng/mL) was observed. These suboptimal levels were also seen in recent reports by Liao et al [31]. Nevertheless, fair correlations between mother and cord blood were found in previous and this study as well [9].…”

Prenatal vitamin D status and respiratory and allergic outcomes in childhood: A meta‐analysis of observational studies

“…From 547 records retrieved by our search, 34 articles published between 2008 and 2017 were finally included (Figure ). Articles are based on 26 separate study populations, including 25 longitudinal birth cohorts and one case‐control study, from 16 different countries (latitude ranging from 55ºN to 31ºS) (Table ).…”

“…Fourteen single studies assessed the association of prenatal 25(OH)D levels with the occurrence of RTIs in the offspring from birth to 36 months of age . Results of the meta‐analysis including available data showed an inverse association between prenatal vitamin D levels and risk of RTIs in offspring.…”

“…29,30,36,47 Circulating 25(OH)D concentrations were measured with diverse methods (Table S2). Ten studies assessed prenatal vitamin D status in maternal plasma or serum collected during pregnancy; one of them did it early in pregnancy (first trimester), 30 six in mid pregnancy (second trimester), 33,43,44,50,52,53 seven in late pregnancy (third trimester), 23,26,31,36,41,45,54 and one study measured vitamin D in all trimesters. 37 Eighteen studies measured vitamin D levels at birth in cord blood samples, 24,25,[27][28][29]32,34,35,[38][39][40]42,[46][47][48][49]55,56 and six studies measured vitamin D at both time points (pregnancy and birth).…”

Vitamin D serostatus and dengue fever progression to dengue hemorrhagic fever/dengue shock syndrome

“…Potential explanatory mechanisms remain speculative. Vitamin D has been related to a decreased anti-inflammatory IL-10 response to viral toll-like receptor-3 stimulation [24]. In addition, some [25] – albeit not all [26] – studies of intracellular infections have suggested that vitamin D may increase dendritic cell expression of CD209, a dengue virus receptor.…”