The protective effect of breast feeding in relation to sudden infant death syndrome (SIDS): I. The effect of human milk and infant formula preparations on binding of toxigenic Staphylococcus aureus to epithelial cells.
Epidemiological studies indicate that breast-fed infants are at a decreased risk of sudden infant death syndrome (SIDS) compared to formula-fed infants. Increasing evidence suggests that infectious agents might be involved in some of these deaths, in particular bacteria which colonise mucosal surfaces and produce superantigenic toxins. One species implicated in recent studies of SIDS infants is Staphylococcus aureus. We tested the hypothesis that in comparison to infant formula, human milk might be a better inhibitor of binding of S. aureus to epithelial cells. In this study, two protocols were used for the binding assays which were assessed by flow cytometry: the in vitro method in which bacteria were treated with milk or formula, washed and added to epithelial cells; and a method more closely reflecting the competitive interactions in vivo in which cells, bacteria, and milk or infant formula were added at the same time. With the in vivo method, breast milk caused enhancement of bacterial binding to cells whilst infant formula caused inhibition; however, for the in vitro method, both human milk and infant formula caused consistent enhancement of binding. Flow cytometry and light microscopy studies indicated that the enhancement was due to the formation of bacterial aggregates. Human milk and infant formula preparations were also compared for components (antibodies or oligosaccharides) that could inhibit binding of S. aureus using the in vitro method. Human milk contained both IgA and IgG. Neither human milk nor infant formula contained oligosaccharides reactive with the Ulex europaeus lectin but both contained components that bound monoclonal antibodies to Lewis(a) and Lewis(b) antigens which can act as receptors for S. aureus. With both methods, synthetic Lewis(a) and Lewis(b) inhibited S. aureus binding in a dose-dependent manner. With human milk, however, the only component which showed a significant correlation with inhibition of binding was the IgA specific for the staphylococcal surface component that binds Lewis(a). Both human milk and infant formula contain components which could potentially inhibit bacterial binding but only breast milk contains the IgA specific for the bacterial adhesin that binds Lewis(a). Studies using the in vivo method suggest that protection associated with breast feeding in relation to SIDS could be due mainly to the formation of bacterial aggregates. The studies have implications for further research into constituents of infant formula.
Saadi
A T
AT
Department of Medical Microbiology, The Medical School, University of Edinburgh, UK.
Gordon
A E
AE
MacKenzie
D A
DA
James
V S
VS
Elton
R A
RA
Weir
D M
DM
Busuttil
A
A
Blackwell
C C
CC
D000328:Adult; D000818:Animals; D001422:Bacterial Adhesion; D001942:Breast Feeding; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000382:microbiology*; D005260:Female; D006801:Humans; D007223:Infant; D007225:Infant Food; D007231:Infant, Newborn; D007983:Lewis Blood Group Antigens / Q000378:metabolism; D008895:Milk, Human / Q000737:chemistry; D013211:Staphylococcus aureus / Q000187:drug effects / Q000378:metabolism*; D013398:Sudden Infant Death / Q000517:prevention & control*; D014407:Tumor Cells, Cultured
D007983:Lewis Blood Group Antigens