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Published on: September 20, 2024
Cord blood vitamin D status impacts innate immune responses
Valencia P Walker1, Xiaoran Zhang, Ida Rastegar
1Department of Pediatrics, Division of Neonatology and Developmental Biology, David Geffen School of Medicine at University of California, Los Angeles, Los Angeles, California 90095, USA. vpwalker@mednet.ucla.edu
Insights
Newborn vitamin D deficiency impairs the antimicrobial response in monocytes. Supplementing with 25-hydroxyvitamin D(3) [25(OH)D(3)] in vitro restored these crucial immune functions, highlighting vitamin D
Area of Science:
- Immunology
- Neonatal Health
- Nutritional Science
Background:
- Vitamin D plays a critical role in immune system regulation.
- Toll-like receptor (TLR) pathways are essential for innate immunity and antimicrobial defense.
- Cord blood vitamin D levels may influence neonatal immune responses.
Purpose of the Study:
- To assess vitamin D concentrations in newborn cord blood.
- To investigate the impact of vitamin D deficiency on TLR-induced antimicrobial responses in neonatal monocytes.
- To determine if in vitro vitamin D supplementation can restore these responses.
Main Methods:
- Measurement of 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] in cord blood from 23 newborns.
- Culture of human monocytes in cord blood plasma.
- Stimulation of monocytes with TLR2 and TLR4 ligands, followed by analysis of antimicrobial gene expression via quantitative PCR.
Main Results:
- Positive correlation observed between cord blood 25(OH)D and 1,25(OH)(2)D concentrations.
- Monocytes from severely vitamin D-deficient plasma showed reduced TLR-induced cathelicidin expression compared to sufficient plasma.
- In vitro supplementation with 25(OH)D(3) enhanced antimicrobial peptide gene expression.
Conclusions:
- Cord blood vitamin D deficiency negatively impacts TLR-induced antimicrobial production in neonatal monocytes.
- Exogenous 25(OH)D(3) supplementation in vitro effectively restored TLR-induced antimicrobial responses.
- Further research is warranted to fully understand vitamin D's role in newborn immunity.
Objectives:
Our objectives were to 1) assess cord blood vitamin D concentrations from healthy term newborns, 2) ascertain whether cord blood vitamin D insufficiency precludes optimal induction of the Toll-like receptor (TLR) antimicrobial pathway in monocytes, and 3) determine whether in vitro supplementation with 25-hydroxyvitamin D(3) [25(OH)D(3)] and/or 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] restores TLR-induced antimicrobial responses.
Study Design:
Plasma concentrations of 25(OH)D and 1,25(OH)(2)D were measured from cord blood of 23 newborns. Human monocytes were cultured in cord blood plasma and stimulated with TLR2 and TLR4 ligands, and then antimicrobial gene expression was analyzed using quantitative PCR.
Results:
Cord blood 25(OH)D and 1,25(OH)(2)D concentrations were positively correlated to each other (r = 0.78; P <0.0001). Compared with those conditioned in vitamin D-sufficient plasma [25(OH)D > 75 nmol/liter], monocytes cultured in severely vitamin D-deficient plasma [25(OH)D < 30 nmol/liter] exhibited decreased TLR-induced cathelicidin expression (P <0.05). Supplementation in vitro of vitamin D-deficient plasma with 25(OH)D(3) increased antimicrobial peptide gene expression.
Conclusions:
Cord blood vitamin D deficiency, by its effects on TLR-induced antimicrobial production, altered in vitro monocyte responses. The observation that exogenous 25(OH)D(3) in vitro recovered TLR-induced antimicrobial responses suggests the need for additional prospective investigations to further delineate the role of vitamin D in the newborn immune response.
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