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Influenza virus infection and bacterial clearance in young adult and aged mice

P R Wyde1, H R Six, M W Ambrose

  • 1Influenza Research Center, Baylor College of Medicine.

Journal of Gerontology
|September 1, 1989
PubMed

Insights

Influenza A (H3N2) virus infection impairs bacterial lung clearance in mice. Aged mice show a more pronounced deficit in clearing Staphylococcus aureus or Serratia marcescens after infection.

Area of Science:

  • Immunology
  • Microbiology
  • Gerontology

Background:

  • Bacterial lung infections can be exacerbated by concurrent viral infections.
  • Influenza A virus (H3N2) is a significant respiratory pathogen.
  • Age-related changes can impact immune responses to infection.

Purpose of the Study:

  • To investigate the impact of influenza A (H3N2) virus infection on the lung clearance of bacteria (Staphylococcus aureus and Serratia marcescens).
  • To compare these effects in young adult and aged mice.

Main Methods:

  • Mice of two age groups (young adult and aged) were infected with influenza A/Hong Kong/68 (H3N2) virus.
  • Following viral infection, mice were challenged with Staphylococcus aureus or Serratia marcescens.
  • Pulmonary bacterial clearance, viral titers, interferon levels, pulmonary histopathology, and immune cell activity were assessed.

Main Results:

  • Virus-infected mice, both young and aged, demonstrated significantly reduced bacterial clearance compared to controls.
  • Aged, virus-infected mice exhibited a more pronounced deficit in bacterial clearance.
  • This enhanced deficit in aged mice did not correlate with viral load, interferon levels, or lung tissue damage.
  • Phagocytic and bactericidal activities of lung immune cells (macrophages and neutrophils) were comparable between infected young and aged mice.

Conclusions:

  • Influenza A (H3N2) virus infection compromises the lung's ability to clear bacteria in a manner that is exacerbated by age.
  • Age-related susceptibility to secondary bacterial pneumonia following influenza may not be solely explained by viral load or immune cell function.

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