Low breast milk TGF-beta2 is induced by Lactobacillus reuteri supplementation and associates with reduced risk of sensitization during infancy.
The immunological composition of breast milk differs between mothers. The reasons for these differences and the consequences for the breast-fed infants are poorly understood. The aim of this study was to evaluate the effect of probiotic Lactobacillus reuteri supplementation on the immunological composition of breast milk in relation to sensitization and eczema in the babies. Total IgA, secretory IgA (SIgA), TGF-beta1, TGF-beta2, IL-10, TNF, soluble CD14 (sCD14), and Na/K ratios were analyzed in colostrum and mature milk obtained from women treated with L. reuteri (n = 54) or placebo (n = 55) from gestational week 36 until delivery. Bacteriological analyses of L. reuteri were performed in faecal samples of the mothers. The infants were followed prospectively for 2 yr regarding development of eczema and sensitization as defined by a positive skin prick test and/or circulating allergen-specific IgE antibodies at 6, 12, and 24 months of age. Supplementation of L. reuteri during pregnancy was associated with low levels of TGF-beta2 and slightly increased levels of IL-10 in colostrum. For TGF-beta2, this association was most pronounced in mothers with detectable L. reuteri in faeces. Infants receiving breast milk with low levels of TGF-beta2 were less likely to become sensitized during their first 2 yr of life. A similar trend was observed for development of IgE-associated eczema. The levels of total IgA, SIgA, TGF-beta1, TNF, sCD14, and Na/K ratios in breast milk were not affected by the intake of L. reuteri. None of these parameters correlated with sensitization or development of eczema in the infant, except for high Na/K ratios that associated with increased risk of sensitization. Supplementation with L. reuteri during late pregnancy reduces breast milk levels of TGF-beta2, and low levels of this cytokine are associated with less sensitization and possibly less IgE-associated eczema in breast-fed infants.
Böttcher
Malin Fagerås
MF
Division of Paediatrics, Department of Molecular and Clinical Medicine, Linköping University, Linköping, Sweden. malfa@imk.liu.se
Abrahamsson
Thomas Robert
TR
Fredriksson
Mats
M
Jakobsson
Ted
T
Björkstén
Bengt
B
D000328:Adult; D001942:Breast Feeding; D003126:Colostrum / Q000737:chemistry* / Q000276:immunology / Q000382:microbiology; D016207:Cytokines / Q000032:analysis* / Q000276:immunology; D004311:Double-Blind Method; D004485:Eczema / Q000276:immunology / Q000517:prevention & control; D005243:Feces / Q000382:microbiology; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology* / Q000517:prevention & control; D007073:Immunoglobulin E / Q000097:blood; D007223:Infant; D007231:Infant, Newborn; D052200:Limosilactobacillus reuteri / Q000276:immunology* / Q000302:isolation & purification; D008895:Milk, Human / Q000737:chemistry / Q000276:immunology* / Q000382:microbiology; D011247:Pregnancy; D019936:Probiotics / Q000008:administration & dosage*; D012307:Risk Factors; D053781:Transforming Growth Factor beta2 / Q000032:analysis*
D016207:Cytokines; D053781:Transforming Growth Factor beta2; D007073:Immunoglobulin E