title: Evaluation of the effects of probiotic supplementation from the neonatal period on innate immune development in infancy.
abstract: BACKGROUND
  Activation of the innate immune system by microbial stimulation is believed to be critical for normal immune maturation, and there has been speculation that these pathways are important for inhibiting allergic-immune responses.
  
  
  OBJECTIVE
  To assess innate immune function following a 6-month supplementation with probiotic bacteria.
  
  
  METHODS
  Two hundred and thirty-one allergic, pregnant women were recruited into a randomized, controlled trial. The infants received either a probiotic (Lactobacillus acidophilus LAVRI-A1; Probiomics) or placebo (maltodextrin alone) daily for the first 6 months of life. Mononuclear cell samples were available from 118 infants. Functional responses to toll-like receptor (TLR) were assessed using ligands for TLR2 (Pansorbin) and TLR4/CD14 [lipopolysaccharide (LPS)] and measuring cytokine responses in the supernatants. Antigen-presenting cell function, as well as capacity for cytokine production (IL-12p70 and IL-10) was assessed.
  
  
  RESULTS
  Infants in the probiotic group did not demonstrate differences in innate immune function compared with those in the control group. No differences were seen when cytokine responses were examined following stimulation with Pansorbin (TLR2) or LPS (TLR4). Similarly, no differences were seen in the antigen-presenting capacity of these infants. The mean fluorescence intensities of human leucocyte antigen-DR (HLA-DR) on monocytes, B cells and dendritic cells (DC) subsets were not affected, nor were the percentage of circulating DC subsets affected by a 6-month supplementation with L. acidophilus LAVRI-A1.
  
  
  CONCLUSIONS
  Probiotic supplementation with L. acidophilus for the first 6 months of life did not alter early innate immune responses in this population at high risk of developing allergic disease.
authors.affiliation: School of Paediatrics and Child Health Research, University of Western Australia, Perth, WA, Australia.
authors.forename: A
authors.initials: A
authors.lastname: Taylor
authors.forename: J
authors.initials: J
authors.lastname: Hale
authors.forename: J
authors.initials: J
authors.lastname: Wiltschut
authors.forename: H
authors.initials: H
authors.lastname: Lehmann
authors.forename: J A
authors.initials: JA
authors.lastname: Dunstan
authors.forename: S L
authors.initials: SL
authors.lastname: Prescott
mesh_terms: D000938:Antigen-Presenting Cells / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D019587:Dietary Supplements; D004311:Double-Blind Method; D004797:Enzyme-Linked Immunosorbent Assay; D005243:Feces / Q000382:microbiology; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D006967:Hypersensitivity / Q000382:microbiology / Q000517:prevention & control*; D007107:Immune System / Q000502:physiology*; D007223:Infant; D007231:Infant, Newborn; D018664:Interleukin-12 / Q000276:immunology; D007779:Lactobacillus acidophilus; D016014:Linear Models; D008070:Lipopolysaccharides / Q000494:pharmacology; D009000:Monocytes / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D019936:Probiotics / Q000008:administration & dosage*; D015398:Signal Transduction; D051195:Toll-Like Receptor 2 / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000378:metabolism
chemical_list: D016207:Cytokines; D006684:HLA-DR Antigens; D008070:Lipopolysaccharides; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D018664:Interleukin-12