Factors enhancing adherence of toxigenicStaphylococcus aureusto epithelial cells and their possible role in sudden infant death syndrome

Abstract

SUMMARYToxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewisa antigen and infection with respiratory syncytial virus (RSVT). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from nonsecretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewisa or anti-type-I precursor significantly reduced bacterial binding (P < 0 01); however, attachment of the bacteria correlated only with the amount of Lewisa antigen detected on the cells (P < 0 01). HEp-2 cells infected with RSV bound significantly more bacteria than uninfected cells. These findings are discussed in context, of factors previously associated with SIDS (mother's smoking, bottle feeding and the prone sleeping position) and a hypothesis proposed to explain some cases of SIDS.

RSV Mediates Pseudomonas aeruginosa Binding to Cystic Fibrosis and Normal Epithelial Cells

“…In addition, a viral infection can be associated with a rise in antipseudomonal antibodies in CF patients with intermittent or chronic pseudomonal colonization, especially in case of RSV infection (14). These findings are furthermore consistent with several studies that demonstrate enhanced adherence of bacteria, like Haemophilus influenzae and Staphylococcus aureus, to epithelial cells after viral infection in vitro (9,18,19) and in vivo (20,21). However, there are only few experimental data about synergism between viruses and P. aeruginosa in inducing infections.…”

Staphylococcus aureus colonization and non-influenza respiratory viruses: Interactions and synergism mechanisms

“…Despite the high incidence of bacterial and RSV co-infection in both children and adults, only few studies aimed to investigate the possible interactions between S. aureus and this virus [87–90]. RSV is supposed to exacerbate S. aureus co-infection via at least two mechanisms: enhancing the adhesion of S. aureus to the RSV-infected cells [88,89], and decreasing the bacterial clearance by altering the immune response to S. aureus [87,90]. …”

“…In vitro studies had shown that RSV-infected epithelial cells bind more S. aureus than uninfected cells [88,89]. Study of nasal washings in patients with respiratory virus diseases has shown that secretion of Lewis blood group antigens is associated with RSV infection [91].…”

“…Study of nasal washings in patients with respiratory virus diseases has shown that secretion of Lewis blood group antigens is associated with RSV infection [91]. In addition, epithelial cells (HEp2) expressing high concentrations of antigens of the Lewis blood group bound significantly more S. aureus than cells expressing low concentrations of these antigens [88,89]. While RSV infects about 50% of infants by the first year of life, Lewis antigen is expressed in secretions of nearly 90% of 3 month-aged infants [88,89].…”

“…In addition, epithelial cells (HEp2) expressing high concentrations of antigens of the Lewis blood group bound significantly more S. aureus than cells expressing low concentrations of these antigens [88,89]. While RSV infects about 50% of infants by the first year of life, Lewis antigen is expressed in secretions of nearly 90% of 3 month-aged infants [88,89]. This may explain the high susceptibility of RSV-infected infants to secondary staphylococcal infection, sometimes resulting in lethal issue [92].…”