In addition to the remarkable reinforcement of mucosal defence provided by maternal SIgA (and SIgM) antibodies as a natural immunological 'substitution therapy', it is important to emphasize the positive nutritional effect of breastfeeding on immune development (Brandtzaeg, 1996b). Also, as mentioned above, breast milk contains a number of immune cells, cytokines and growth factors that may exert a significant biological effect in the suckling's gut, apparently enhancing in an indirect way even the long-term health of the individual (Wold and Hanson, 1994; Newman, 1995).
Numerous studies of the effect of breast-feeding on secretory immunity have been performed with salivary IgA measurements as a read-out system. Discrepant observations have been made, probably to some extent reflecting different cytokine levels in the milk as discussed above. The influence of contaminating the saliva sample with milk SIgA, shielding of the suckling's mucosal immune system by maternal SIgA antibodies, and altered growth and composition of the infant's gut flora have been discussed as additional uncontrollable variables (Brandtzaeg et al., 1991). However, the balance of accumulated data suggests that breast-feeding promotes the post-natal development of secretory immunity (Wold and Hanson, 1994; Brandtzaeg, 1998), apparently even in the urinary tract (Newman, 1995); and there are reports of enhanced secretory, as well as systemic, immune responses to oral and parenteral vaccines in breastfed babies (Hahn-Zoric et al., 1990; Pabst and Spady, 1990).
Nevertheless, several prospective studies have reported that the early physiological increase of salivary IgA (and IgM) is more prominent in formula-fed than in solely breast-fed infants (Gleeson et al., 1986; Stephens, 1986; Brandtzaeg et al., 1991), although this difference seems to disappear after weaning (Tappuni and Challacombe, 1994). It likewise seems that breast-feeding, in comparison with formula-feeding, reduces the salivary IgA antibody titres to cow's milk proteins; this decrease was seen after a nursing period of only 3 weeks and appeared also in infants receiving mixed feeding (Gleeson et al., 1986; Renz et al., 1991). Altogether, therefore, although breast-feeding initially appears to reduce induction of salivary IgA, it will later on in infancy (up to 8 months) boost this response (Avanzini et al., 1992; Fitzsimmons et al., 1994). In a similar manner, experiments in mice have demonstrated that SIgA antibodies from breast milk affect the stimulatory properties of the gut flora in the suckling by retarding bacterial contact with the developing GALT (Cebra et al., 1999). When the host's mucosal immune response subsequently is successfully elicited, GALT will be further shielded by the SIgA antibodies produced in the gut; local immunostimulation is thereby attenuated despite the continued presence of microorganisms (Shroff et al., 1995). This could contribute to the hypo-responsiveness or tolerance that normally exists towards members of the autologous commensal gut bacteria, in both rodents and humans (Helgeland and Brandtzaeg, 2000).
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