| Summary: | The objectives of the study were: (1) to determine if there is a similar pattern of enhanced binding of <I>Neisseria meningitidis</I>, <I>Haemophilus influenzae </I>type b, <I>Staphylococcus aureus, </I>and <I>Bordetella pertussis</I> to RSV subgroup B infected cells as observed with RSV subgroup A infection; (2) to determine if there is increased binding of other species of bacteria associated with meningitis and those associated with secondary respiratory infections or exacerbation of chronic bronchitis to RSV infected cells; (3) to determine if there was similar pattern of increased bacterial binding to influenza virus infected cells; (4) to determine if as with RSV infected cells there was an increase in expression of native cell surface antigens which can act as receptors for bacteria; (5) to determine if there is enhanced binding of bacteria associated with meningitis or respiratory disease to cells of smokers; (6) to assess cells of smokers and non-smokers for differences in levels of antigens proposed to act as bacterial receptors. With the exception of an antibiotic-sensitive strain of <I>Moraxella catarrhalis</I> (MC2) infection of an epithelial cell line (HEp-2) with RSV (subgroups A or B) enhanced binding of all bacterial strains tested. Compared with the antibiotic resistant strain, MC2 and other antibiotic-sensitive isolates of <I>M. catarrhalis</I> were found to express differences in outer membrane proteins, sensitivity to complement-mediated killing, phagocytosis and intracellular survival. Cells infected with human influenza A virus showed increased adherence of each of the species tested, including the antibiotic-sensitive isolates of <I>M. catarrhalis</I>. Compared with uninfected cells, influenza virus infected HEp-2 cells showed significantly increased binding of monoclonal antibodies for the cell surface antigens CD14 and CD18 that can act as receptors for some bacteria. Pre-treatment of HEp-2 cells with neuraminidase showed increased bacterial binding compared with untreated HEp-2 cells, but the increase was less than that observed for influenza infected cells. The results suggest that while smoking is a predisposing factor for viral infection, it can enhance bacterial binding of strains associated with meningitis or respiratory infection on its own.
|
|---|
