title: Binding of bacteria to HEp-2 cells infected with influenza A virus.
abstract: Epidemiological studies indicate influenza virus infection increases susceptibility to bacterial respiratory pathogens and to meningococcal disease. Because density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use flow cytometry methods for assessment of bacterial binding and detection of cell surface antigens to determine: (1) if HEp-2 cells infected with human influenza A virus bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptors for bacterial binding; (3) if neuraminidase affects binding of bacteria to HEp-2 cells. There was significantly increased binding of all isolates tested regardless of surface antigen characteristics. There were no significant differences between virus-infected and -uninfected Hep-2 cells in binding of monoclonal antibodies to Lewisb, Lewisx or H type 2. There were significant increases in binding of monoclonal antibodies to CD14 (P < 0.05) and CD18 (P < 0.01). Treatment of cells with monoclonal antibodies significantly reduced binding of Neisseria meningitidis strain C:2b:P1.2, CD14 (P < 0.001) and CD18 (P < 0.001). No reduction in binding of a strain of Streptococcus pneumoniae (12F) was observed in these experiments. Neuraminidase treatment of HEp-2 cells increased binding of monoclonal antibodies to CD14 (P < 0.01) and CD18 (P < 0.01). In three experiments, the increase in binding of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was significant (P < 0.05).
authors.affiliation: Department of Medical Microbiology, University of Edinburgh, UK.
authors.forename: O R
authors.initials: OR
authors.lastname: El Ahmer
authors.forename: M W
authors.initials: MW
authors.lastname: Raza
authors.forename: M M
authors.initials: MM
authors.lastname: Ogilvie
authors.forename: D M
authors.initials: DM
authors.lastname: Weir
authors.forename: C C
authors.initials: CC
authors.lastname: Blackwell
mesh_terms: D000818:Animals; D000954:Antigens, Surface / Q000096:biosynthesis; D001422:Bacterial Adhesion / Q000502:physiology*; D018821:CD18 Antigens / Q000378:metabolism; D002460:Cell Line; D004285:Dogs; D006090:Gram-Negative Bacteria / Q000502:physiology*; D006094:Gram-Positive Bacteria / Q000502:physiology*; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D009345:Neisseria meningitidis / Q000502:physiology; D009439:Neuraminidase / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D000954:Antigens, Surface; D018821:CD18 Antigens; D018950:Lipopolysaccharide Receptors; D009439:Neuraminidase