title: Cord blood vitamin D status impacts innate immune responses.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
authors.affiliation: Department 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
authors.forename: Valencia P
authors.initials: VP
authors.lastname: Walker
authors.forename: Xiaoran
authors.initials: X
authors.lastname: Zhang
authors.forename: Ida
authors.initials: I
authors.lastname: Rastegar
authors.forename: Philip T
authors.initials: PT
authors.lastname: Liu
authors.forename: Bruce W
authors.initials: BW
authors.lastname: Hollis
authors.forename: John S
authors.initials: JS
authors.lastname: Adams
authors.forename: Robert L
authors.initials: RL
authors.lastname: Modlin
mesh_terms: D000368:Aged; D002478:Cells, Cultured; D005260:Female; D005312:Fetal Blood / Q000276:immunology* / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology*; D007231:Infant, Newborn; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D014807:Vitamin D / Q000097:blood* / Q000276:immunology; D014808:Vitamin D Deficiency / Q000097:blood / Q000276:immunology*
chemical_list: D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D014807:Vitamin D