title: The protective effect of breast feeding in relation to sudden infant death syndrome (SIDS): II. The effect of human milk and infant formula preparations on binding of Clostridium perfringens to epithelial cells.
abstract: Breast feeding is known to protect an infant against gastrointestinal pathogens and epidemiological studies indicate that compared to breast fed infants, formula fed infants are at a greater risk of dying from sudden infant death syndrome (SIDS). Many SIDS infants have symptoms of gastrointestinal infections prior to death and one gastrointestinal pathogen associated with SIDS is Clostridium perfringens. Studies have found that a significantly higher number of formula fed SIDS infants have C perfringens and its enterotoxin in their faeces compared to breast fed infants. The aim of the study was to compare the effects of human milk and infant formula on binding of C perfringens to epithelial cells. Two protocols were used to assess the effect of human milk and infant formula to inhibit binding of C perfringens to epithelial cells. Binding was assessed by flow cytometry. For the in vivo protocol which more closely represents interactions on the mucosal surface, breast milk enhanced bacterial binding but infant formula caused inhibition of binding; however for the in vitro method, both human milk and infant formula resulted in consistent enhancement of binding. Flow cytometry studies indicated that enhancement of binding was due to the formation of bacterial aggregates. Lewis(a) and Lewis(b) antigens, found in both breast milk and infant formula, inhibited C. perfringens binding in a dose dependent manner. The Lewis(a) and Lewis(b) antigens in human milk and infant formula can inhibit C. perfringens binding to epithelial cells. While infant formula reduced binding of C. perfringens to epithelial cells in the experiments carried out with the in vivo protocol, the protective effects of breast feeding in relation to colonisation with C. perfringens are more likely to be due to formation of bacterial aggregates. These findings have implications for improving infant formula preparations.
authors.affiliation: Department of Medical Microbiology, The Medical School, University of Edinburgh, UK.
authors.forename: A E
authors.initials: AE
authors.lastname: Gordon
authors.forename: A T
authors.initials: AT
authors.lastname: Saadi
authors.forename: D A
authors.initials: DA
authors.lastname: MacKenzie
authors.forename: V S
authors.initials: VS
authors.lastname: James
authors.forename: R A
authors.initials: RA
authors.lastname: Elton
authors.forename: D M
authors.initials: DM
authors.lastname: Weir
authors.forename: A
authors.initials: A
authors.lastname: Busuttil
authors.forename: C C
authors.initials: CC
authors.lastname: Blackwell
mesh_terms: D000818:Animals; D001422:Bacterial Adhesion; D001942:Breast Feeding; D003016:Clostridium perfringens / Q000378:metabolism*; D004847:Epithelial Cells / Q000382:microbiology*; D006801:Humans; D007223:Infant; D007225:Infant Food; D007231:Infant, Newborn; D007983:Lewis Blood Group Antigens / Q000378:metabolism; D008895:Milk, Human / Q000737:chemistry; D013398:Sudden Infant Death / Q000517:prevention & control*; D014407:Tumor Cells, Cultured
chemical_list: D007983:Lewis Blood Group Antigens