title: Developmental and environmental factors that enhance binding of Bordetella pertussis to human epithelial cells in relation to sudden infant death syndrome (SIDS).
abstract: Asymptomatic infection due to Bordetella pertussis has been suggested to be one cause of sudden infant death syndrome (SIDS). We examined developmental and environmental factors previously found to affect binding of another toxigenic species, Staphylococcus aureus, to human epithelial cells: expression of the Lewis(a) antigen; infection with respiratory syncytial virus (RSV); exposure to cigarette smoke; and the inhibitory effect of breast milk on bacterial binding. Binding of two strains of B. pertussis (8002 and 250825) to buccal epithelial cells was significantly reduced by treating the cells with monoclonal antibodies to Lewis(a) (P < 0.05) and Lewis(x) (P < 0.01) antigens. Both strains bound in significantly greater numbers to cells from smokers compared with cells from non-smokers (P < 0.05). HEp-2 cells infected with RSV subtypes A or B had higher binding indices for both 8002 (P < 0.001) and 250825 (P < 0.01). On RSV-infected cells, there was significantly enhanced binding of monoclonal antibodies to Lewis(x) (P < 0.05), CD14 (P < 0.001) and CD18 (P < 0.01); and pre-treatment of cells with anti-CD14 or CD18 also significantly reduced binding of both strains of B. pertussis. Pre-treatment of the bacteria with human milk significantly reduced their binding to epithelial cells. The results are discussed in relation to our three-year survey of bacterial carriage among 253 healthy infants, their mothers and local SIDS cases between 1993-1995 and in relation to the change to an earlier immunisation schedule for infants and the recent decline in SIDS in Britain.
authors.affiliation: Department of Medical Microbiology, University of Edinburgh, UK.
authors.forename: A T
authors.initials: AT
authors.lastname: Saadi
authors.forename: C C
authors.initials: CC
authors.lastname: Blackwell
authors.forename: S D
authors.initials: SD
authors.lastname: Essery
authors.forename: M W
authors.initials: MW
authors.lastname: Raza
authors.forename: O R
authors.initials: OR
authors.lastname: el Ahmer
authors.forename: D A
authors.initials: DA
authors.lastname: MacKenzie
authors.forename: V S
authors.initials: VS
authors.lastname: James
authors.forename: D M
authors.initials: DM
authors.lastname: Weir
authors.forename: M M
authors.initials: MM
authors.lastname: Ogilvie
authors.forename: R A
authors.initials: RA
authors.lastname: Elton
authors.forename: A
authors.initials: A
authors.lastname: Busuttil
authors.forename: J W
authors.initials: JW
authors.lastname: Keeling
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology; D001419:Bacteria / Q000302:isolation & purification; D001422:Bacterial Adhesion; D001886:Bordetella pertussis / Q000472:pathogenicity*; D018821:CD18 Antigens / Q000276:immunology; D002353:Carrier State / Q000453:epidemiology / Q000382:microbiology; D002478:Cells, Cultured; D004848:Epithelium / Q000382:microbiology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007983:Lewis Blood Group Antigens / Q000096:biosynthesis / Q000276:immunology; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D008895:Milk, Human / Q000276:immunology; D018357:Respiratory Syncytial Virus Infections / Q000150:complications; D012189:Retrospective Studies; D012907:Smoking / Q000009:adverse effects; D013398:Sudden Infant Death / Q000453:epidemiology / Q000209:etiology*
chemical_list: D000911:Antibodies, Monoclonal; D018821:CD18 Antigens; D007983:Lewis Blood Group Antigens; D018950:Lipopolysaccharide Receptors