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Binding of bacteria to HEp-2 cells infected with influenza A virus
O R El Ahmer1, M W Raza, M M Ogilvie
1Department of Medical Microbiology, University of Edinburgh, UK.
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).
Insights
Influenza infection enhances bacterial binding to respiratory cells by altering cell surface receptors like CD14 and CD18. This increased susceptibility highlights a key mechanism in secondary bacterial infections following flu.
Area of Science:
- Microbiology
- Virology
- Immunology
Background:
- Influenza virus infection is known to increase susceptibility to secondary bacterial infections.
- Bacterial colonization density is a critical factor in disease development.
- Understanding host-pathogen interactions post-influenza is crucial for preventing secondary infections.
Purpose of the Study:
- To quantify bacterial binding to HEp-2 cells infected with influenza A virus.
- To investigate if influenza infection alters cell surface antigen expression.
- To determine the role of neuraminidase in bacterial adherence to host cells.
Main Methods:
- Flow cytometry was employed to assess bacterial binding to HEp-2 cells.
- Detection of cell surface antigens using monoclonal antibodies.
- Evaluation of bacterial adherence following neuraminidase treatment.
Main Results:
- Influenza A virus-infected HEp-2 cells showed significantly increased binding of tested bacterial isolates.
- Influenza infection led to increased expression of CD14 and CD18 on HEp-2 cells.
- Neuraminidase treatment also increased CD14 and CD18 expression, enhancing Staphylococcus aureus binding.
Conclusions:
- Influenza infection promotes bacterial adherence to respiratory epithelial cells.
- Upregulation of CD14 and CD18 by influenza and neuraminidase contributes to increased bacterial binding.
- These findings elucidate mechanisms underlying enhanced susceptibility to bacterial pathogens post-influenza.