41

BREASTFEEDING AND ATOPIC

SENSITISATION

Marko Kalliomki and Erika Isolauri

Department of Paediatrics, Turku University Hospital, 20520 Turku, Finland

1. INTRODUCTION
Atopic disease may manifest itself even during exclusive breastfeeding1.
This early sensitisation has been explained by the presence in breastmilk of
maternal dietary antigens in low amounts2,3. However, the concentrations of
dietary antigens in breastmilk do not differ between the mothers feeding
atopic and normal infants3 which apparently explains why the effects of
maternal elimination diets during lactation on the development of atopic
sensitisation have been controversial4. Moreover, these diets may entail
nutritional risks for both the mother and the infant5. Consequently, maternal
dietary restrictions during lactation for primary allergy prevention are not
recommended. The data imply that atopic sensitisation during exclusive
breastfeeding may depend more on immunological factors than the presence
of dietary antigens in breastmilk.

2. MECHANISMS OF ORAL TOLERANCE

Oral tolerance is a systemic unresponsiveness to orally administered non-
pathogenic antigen. Immunological mechanism of oral tolerance is
dependent on the dose of antigen6. High doses of antigen result the clonal
anergy and/or deletion whereas low-dose antigen feeding is characterised by
the induction of regulatory T cells producing suppressor cytokines such as
transforming growth factor beta (TGF ). A recent study clues that the latter

Short and Long Term Effects of Breast Feeding on Child Health

Edited by Berthold Koletzko et al., Kluwer Academic/Plenum Publishers, 2000 389
390 M. Kalliomki andE. Isolauri

mechanism may occur in breastfed infants receiving dietary peptides present

in breastmilk7.

3. TGF- IN BREASTMILK
Human milk contains TGF-1 andTGF-28. In addition to oral tolerance,
TGF- has been shown to have an important impact on the other essential
part of the mucosal immune system, namely IgA production9. Both the
number of IgA-containing cells and the production of TGF- in intestinal
mucosa increase with age10,11. Therefore, the impact of TGF- in breastmilk
may culminate at an early age, when new antigens are first encountered by
the enteral route and the production ofendogenous TGF- and IgA in the gut
are minimal. In a recent study we showed that the concentrations of both
TGF-1 and TGF-2 were higher in colostrum of mothers whose infants
developed atopic disease after weaning compared with those with a
preweaning onset atopic disease12. Moreover, high TGF- in maternal
colostrum was associated with the infant's ability to produce specific IgA in
response to betalactoglobulin, casein, ovalbumin and gliadin, the dietary
antigens most frequently responsible for sensitising the infant.

4. CONCLUSION
The results suggest that TGF- in colostrum may prevent the
development of atopic disease during exclusive breastfeeding and promote
specific IgA production in man.

REFERENCES
1. Isolauri E, et al. (1999) J Pediatr 13427-32.
2. Kilshaw PJ, et al. (1984) Int Arch Allergy Appl Immunol75:8-15.
3. Cant A, et al. (1985) BMJ 291:932-935.
4. Zeiger RS (1999) Immunol Allergy Clin North Am 19:619-646.
5. Arvola T, et al. (1999) Ann Med 31:293-298.
6. Strober W, et al. (1998) J Clin Immunol 18: 1-30.
7. Pecquet S, et al. (1999) Immunology 96:278-285.
8. Saito S, et al. (1993) Clin Exp Immunol94:220-224.
9. Stavnezer J (1995) J Immunol 155:1647-1651.
10. Perkki M, et al. (1980) Pediatr Res 14:953-955.
11. Penttil IA, et al. (1998) Pediatr Res 44:524431.
12. Kalliomki M, et al. (1999) J Allergy Clin Immunol 1999;104:x-y (in press).