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Title: Factors enhancing adherence of toxigenic bacteria to epithelial cells in relation to sudden infant death syndrome
Author: Saadi, Abdulrahman Towfeeq
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1995
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This study tests the hypothesis that the Lewisa antigen, expressed by 80-90% of infants between the ages of 2-4 months, is one of the host receptors for two toxigenic bacteria species suggested to be involved in cot death, Staphylococcus aureus and Bordetella pertussis. Although respiratory viruses are often isolated from SIDS infants, there is no direct evidence for their involvement in these deaths; however, this study examined the effect of virus infection on binding of S. aureus and B. pertussis to epithelial cells in culture. By flow cytometry, binding of three toxigenic strains of S. aureus to buccal epithelial cells (BEC) from non-secretors (which usually express large amounts of Lewisa) was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewisa, anti-type 1 precursor or anti-Lewisx significantly reduced bacterial binding; and binding of S. aureus was significantly correlated with the amount of Lewisa present on the epithelial cells. Binding of B. pertussis to epithelial cells was also significantly inhibited by pre-treatment of the cells with anti-Lewisa or anti-Lewisx. A 67 kDa protein was isolated from cell membrane preparations of S. aureus (NCTC 10655) by affinity adsorption with synthetic Lewisa antigen conjugated to Synsorb beads. Pre-treatment of BEC with the purified protein reduced binding of staphylococcal strains to a greater extent than with the material not bound to the Synsorb beads. Respiratory Syncytial Virus (RSV) infects about 50% of infants by the first year of life and it is often isolated from infants with SIDS. RSV-infected HEp-2 cells bound significantly more S. aureus or B. pertussis than uninfected cells.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available