Maternal antigen stimulation downregulates via mother's milk the specific immune responses in young mice.
BACKGROUND
Different aspects of the vertical transfer of predisposition to allergy from mother to child have been investigated. An issue which is still largely open is the influence of breast-feeding by allergic mothers on the development of the allergic phenotype of the infant. In the current study we employed a murine ovalbumin (OVA) immunization model to investigate possible milk-borne influences of the mother's specific immune status on the primary immune response of the breast-fed pup.


METHODS
Naïve and OVA-immunized female mice were mated simultaneously. Immediately after birth litters were exchanged between the immunized and the untreated mothers which allowed the evaluation of maternal influence exerted via milk only. At the age of 3 weeks the pups were injected with a single dose of OVA intraperitoneally and sacrificed 2 weeks later. Serum was obtained for the determination of total and OVA-specific IgE and IgG2a. In addition, lymphocyte proliferation was measured following OVA stimulation of the pups' splenocytes and lymph node cells. During the lactation period milk was collected from the mothers for evaluation of its total and OVA-specific immunoglobulin levels.


RESULTS
Breast-feeding of naïve pups by OVA-immunized mothers results in the suppression of the pups' specific IgE response as well as the downregulation of the OVA-induced proliferative response of the pups' lymph node cells and splenocytes. Additionally, splenocytes of naïve pups nursed by immune mothers show a decrease in IL-4 production compared to naïve pups nursed by naïve mothers, whereas the IFN-gamma production is not altered.


CONCLUSIONS
We demonstrated the suppression of the pups' primary humoral and cellular response towards OVA by breast-feeding by mothers exposed to OVA shortly before pregnancy. It appears that such a transfer of the suppressive activity from mother to pups via milk directs the pups' immune response towards a Th1 and away from a Th2 type, thus avoiding the 'allergic' phenotype. Our study suggests that breast-feeding by mothers immune to an antigen may suppress the development of an allergic response to this antigen.
Bednar-Tantscher
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Novartis Forschungsinstitut, Vienna, Austria.
Mudde
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D000818:Animals; D000918:Antibody Specificity; D000941:Antigens / Q000276:immunology*; D001942:Breast Feeding; D016207:Cytokines / Q000096:biosynthesis; D015536:Down-Regulation; D005260:Female; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000517:prevention & control; D007114:Immunization; D007073:Immunoglobulin E / Q000032:analysis; D007074:Immunoglobulin G / Q000032:analysis; D008213:Lymphocyte Activation; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008892:Milk / Q000276:immunology*; D023421:Models, Animal; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology*
D000941:Antigens; D016207:Cytokines; D007074:Immunoglobulin G; D007073:Immunoglobulin E; D010047:Ovalbumin