Abstract Title:

Transforming growth factor-beta in breast milk: a potential regulator of atopic disease at an early age.

Abstract Source:

J Allergy Clin Immunol. 1999 Dec;104(6):1251-7. PMID: 10589009

Abstract Author(s):

M Kalliomäki, A Ouwehand, H Arvilommi, P Kero, E Isolauri

Article Affiliation:

Departments of Paediatrics and Biochemistry and Food Chemistry, University of Turku, Finland.


BACKGROUND: According to data from animal and in vitro studies, transforming growth factor-beta (TGF-beta) has a crucial effect on 2 essential parts of the mucosal immune system: IgA production and oral tolerance induction.

OBJECTIVE: We sought to ascertain whether TGF-beta in breast milk is associated with specific IgA production and atopic disease in human subjects.

METHODS: Forty-seven infants with several atopic family members were followed during their first year of life. The concentrations of TGF-beta1 and TGF-beta2 in maternal colostrum, mature milk, and the infants' sera were determined. The enzyme-linked immunospot assay was used to assess the infants' specific IgA production in response to beta-lactoglobulin, casein, gliadin, and ovalbumin.

RESULTS: At 12 months, atopic dermatitis was confirmed in 29 of 47 infants; in 11, atopic disease had begun during exclusive breast-feeding (preweaning onset), whereas in 18 the disease manifested itself after weaning (postweaning onset). The concentrations of both TGF-beta1 and TGF-beta2 were higher in maternal colostrum, but not in mature milk and infants' serum, in infants with postweaning-onset atopic disease compared with those with preweaning-onset disease (P =.0008 and P =. 015, respectively). The concentration of TGF-beta2 was, and that of TGF-beta1 tended to be, higher in the colostrum of mothers whose infants had specific IgA-secreting cells at 3 months in response to at least one of the dietary antigens tested compared with those who did not have such cells (P =.048 and P =.076, respectively).

CONCLUSION: TGF-beta in colostrum may prevent the development of atopic disease during exclusive breast-feeding and promote specific IgA production in human subjects.

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