The Influence Of Maternal Immunity

The immune system of the newborn infant is influenced by maternal immunity, both transplacentally and via the breast milk. Thus, there is a close immunological interaction between the mother and her baby during gestation and during the period of breast-feeding, where the mother may provide protective factors and immune modifying components, as well as antigenic stimulation.

As already discussed, the fetomaternal interface is surrounded by high levels of the Th2 cytokines IL-4 and IL-10 2, probably in order to divert the maternal immune response away from damaging Th1-mediated immune responses30 The tendency of atopics to express Th2-like immunity may thus be of reproductive advantage, and we have recently observed a higher number of children among atopic mothers as compared to non-atopic mothers31. The higher cord blood IgE levels seen in newborns of atopic mothers as compared to newborns with a paternal or no atopic history may depend on a possibly stronger placental Th2 shiftin atopic mothers. The Th2 polarisation during pregnancy may influence the offspring for variable periods postnatally, as evidenced by the selective expansion of Th2 memory cells in antigen challenged newborn mice32. This could conceivably explain the well known higher penetration of maternal than paternal heredity of allergic disease.

Maternal IgG antibodies are transplacentally transferred via an active transport, providing a passive protection for infections in the baby. High levels of cord blood IgG antibodies to P -lactoglobulin have been reported to protect against the development ofcow's milk allergy, although this was not confirmed in another study33 Low levels of IgG antibodies to cat and birch in cord blood are associated with an increased prevalence of sensitvityto cat, as well as asthma at 8 years of age34 .If high levels of maternal allergen-specific IgG antibodies indeed are protective, this may be an alternative explanation to the observations in several epidemiological studies showing an increased risk for allergy to seasonal allergens in children born before the relevant pollen6-7. Birth at this time of the year would provide low levels of cord serum IgG antibodies. Furthermore, high levels of IgG anti-IgE antibodies in cord blood are associated with less allergy during the first 18 months of life, particularly in babies with a strong family history ofallergy35.

The precise relation between breast-feeding and infant allergy is poorly understood. Any allergy-preventing effect of human milk, if true, seems to be limited to babies with a genetically determined increased risk for atopic disease36.The capacity to influence infant immunity may also vary between mothers. Breast milk cell supernatants from atopic mothers stimulate higher levels of cord blood IgE secretion in vitro than cell supernatants from non-atopic mothers37. We have recently been able to demonstrate that breast-milk from non-atopic mothers contain higher levels of ovalbumin-specific secretory IgA antibodies than breast-milk from atopic mothers, as measured by a sensitive enzyme amplified ELISA (Casas etal, unpublished).

During early infancy there is a close immunological interaction between the mother and her offspring, through the breast milk but relatively little is known about the exchange ofimmunological information. Besides numerous components that help in the protection against infection, human milk contains components that enhance the maturation of the immune system of the new-born infant. Observations include an early stimulation of IgA antibody synthesis in breast-fed infants38 and transfer of cell-mediated immunity and cytokines39. Thus, human milk would not only provide passive protection against infections, but also actively stimulate infant immunity. There are considerable individual variations in the composition of human milk, however. This may explain the controversy with regard to the possible allergy-preventive effects of breast feeding. If individual variations in the milk modulate the development of immunity in the neonate, then maternal immunity may represent an environmental factor, which would influence the risk for allergic manifestations in her child, possibly even several years later.

Human milk also contains foreign antigens, e. g. food antigens eaten by the mother and these may sensitise the baby40. A maternal hypoallergenic diet during the lactation period is associated with less atopic eczema in the children, but does not reduce the prevalence of other atopic manifestations during the first four years of life41.

Low levels of total IgA and cow's milk specific IgA42-43in breast milk have been reported to be associated with cow's milk allergy in the infants. This was not confirmed, however, in a carefully controlled prospective study44.

There are several reports in the literature suggesting that allergic disease is associated with an abnormal metabolism of long chain fatty acids. A disturbed composition of polyunsaturated fatty acids (PUFA) has been reported in milk from mothers of atopic infants. For example, the levels of the essential fatty acid linoleic acid (LA), as well as its metabolites were lower in early mature milk from atopic, as compared to non-atopic mothers and the ratio between n-6 and n-3 fatty acids was higher45. Differences in the fatty acid composition of human milk seems to have a relevance for the breast fed infants. Thus, lower levels ofthe n-3 fatty acids, EPA DPA and DHA have been observed in mothers of infants who developed allergic disease during the first year of life as compared to mothers ofbabies who did not develop any allergic manifestation46. These differences were independent ofmaternal allergy. Similarly low levels ofcertain polyamines have been observed in milk from atopic mothers39. As these compounds are required for optimal DNA synthesis, variations in the levels could affect immune responses to foreign antigens in breast fed infants.

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