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Influenza type A virus-mediated adherence of type 1a group B streptococci to mouse tracheal tissue in vivo
Abstract:
Influenza type A virus-mediated adherence of pathogenic bacteria to the mucosal surface of the respiratory tract may be one of several mechanisms whereby influenza predisposes to bacterial pneumonia. In the present study, we quantified the adherence of intranasally administered type 1a group B streptococci to the tracheal tissue of influenza type A/PR8/34 (HONI) virus-infected and mock-infected mice. Influenza type A/PR8/34 virus infection effected a 120-fold increase in the adherence of type 1a group B streptococci to tracheal tissue relative to that observed in mock-infected mice. Adherence of type 1a group B streptococci to the trachea of influenza type A/PR8/34 virus-infected mice was reduced by more than 90% by prior intranasal instillation of chicken antiserum to influenza type A/PR8/34 virus, whereas virtually no reduction in adherence was noted with normal chicken serum or rabbit antiserum to herpes simplex virus type 2. These findings suggest that adherence of type 1a group B streptococci to the tracheal tissue of influenza type A/PR8/34 virus-infected mice is effected by a viral component(s).
Insights
Influenza A virus significantly increases bacterial adherence to the respiratory tract. This viral component-mediated adherence of group B streptococci to the trachea suggests a mechanism for influenza-associated pneumonia.
Area of Science:
- Microbiology
- Virology
- Immunology
Background:
- Influenza virus infection can predispose individuals to secondary bacterial pneumonia.
- The precise mechanisms by which influenza enhances bacterial susceptibility are not fully understood.
- Bacterial adherence to respiratory mucosa is a critical early step in infection.
Purpose of the Study:
- To quantify the adherence of Streptococcus agalactiae (group B streptococci) to mouse tracheal tissue during influenza A virus infection.
- To investigate the role of viral components in mediating this enhanced bacterial adherence.
Main Methods:
- Mice were infected with influenza A/PR8/34 (HON1) virus or mock-infected.
- Intranasal administration of type 1a group B streptococci was performed.
- Bacterial adherence to tracheal tissue was quantified.
- The effect of specific antisera (chicken anti-influenza A, normal chicken serum, rabbit anti-HSV-2) on bacterial adherence was assessed.
Main Results:
- Influenza A/PR8/34 virus infection resulted in a 120-fold increase in type 1a group B streptococci adherence to tracheal tissue compared to mock-infected controls.
- Pre-instillation of chicken antiserum against influenza A/PR8/34 virus reduced bacterial adherence by over 90%.
- Normal chicken serum and rabbit antiserum to herpes simplex virus type 2 did not significantly reduce adherence.
Conclusions:
- Influenza A virus infection dramatically enhances the adherence of type 1a group B streptococci to the respiratory tract.
- These findings strongly suggest that a viral component(s) of influenza A virus mediates this increased bacterial adherence.
- This mechanism likely contributes to the increased risk of bacterial pneumonia following influenza infection.
