Format

Send to

Choose Destination
Br J Nutr. 2013 Jun;109(11):1962-70. doi: 10.1017/S0007114512004229. Epub 2012 Oct 30.

Immunological programming by breast milk creates an anti-inflammatory cytokine milieu in breast-fed infants compared to formula-fed infants.

Author information

1
Department of Paediatrics, Turku University Hospital, Kiinamyllynkatu 4-8, Turku 20520, Finland.

Abstract

Breast milk provides important maturational stimuli to an infant's developing immune system. However, data concerning the role of breast-feeding in reducing the risk of allergic disease remain contradictory. Previous studies have centred on comparative analyses of breast milk and formula compositions. We chose a slightly different angle, whereby we focused on the effects of the chosen diet on the infant himself, comparing the immune development of formula-fed and breast-fed children. The objective of the present study was to determine how the mode of feeding affects infant immunology. Altogether, eighteen formula-fed infants with limited breast-feeding for ,3 months and twenty-nine infants who were exclusively breast-fed for .3 months were included in the study. Concentrations of interferon g, TNF-a IL-10, IL-5, IL-4 and IL-2 were measured simultaneously from the same serum sample through use of a multiplexed flow cytometric assay at the ages of 1, 3, 6 and 12 months. Transforming growth factor β2 (TGF-β2) was measured using ELISA at the same time points. Serum TNF-a and IL-2 concentrations were significantly higher in formula-fed than in breast-fed infants during the first year of life (ANOVA, P=0·002). The serum concentrations of TGF-b were significantly lower in formula-fed than in breast-fed infants throughout the first year of life (ANOVA, P≤0·0001). Exclusive breast-feeding promotes an anti-inflammatory cytokine milieu, which is maintained throughout infancy. Such an immunological environment limits hyper-responsiveness and promotes tolerisation, possibly prohibiting the onset of allergic disease.

PMID:
23110822
DOI:
10.1017/S0007114512004229
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Cambridge University Press
Loading ...
Support Center