Binding of bacteria to HEp-2 cells infected with influenza A virus

Epidemiological studies indicate influenza virus infection increases suscep tibility to bacterial respiratory pathogens and to meningococcal disease. B ecause density of colonisation is an important factor in the development of bacterial disease, the objectives of the study were to use now cytometry m ethods for assessment of bacterial binding and detection of cell surface an tigens to determine: (1) if HEp-2 cells infected with human influenza A vir us bind greater numbers of bacteria than uninfected cells; (2) if influenza infection alters expression of cell surface antigens which act as receptor s for bacterial binding; (3) if neuraminidase affects binding of bacteria t o HEp-2 cells. There was significantly increased binding of all isolates te sted regardless of surface antigen characteristics. There were no significa nt differences between virus-infected and -uninfected Hep-2 cells in bindin g of monocional antibodies to Lewis(b), Lewis(x) or H type 2. There were si gnificant increases in binding of monoclonal antibodies to CD14 (P < 0.05) and CD18 (P < 0.01). Treatment of cells with monoclonal antibodies signific antly 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 Strept ococcus pneumoniae (12F) was observed in these experiments. Neuraminidase t reatment 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 bindi ng of meningococcal strain C:2b:P1.2 to neuraminidase-treated cells was not significant, but binding of Staphylococcus aureus strain NCTC 10655 was si gnificant (P < 0.05). (C) 1999 Federation of European Microbiological Socie ties. Published by Elsevier Science B.V. All rights reserved.