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Influenza promotes pneumococcal growth during coinfection by providing host sialylated substrates as a nutrient

Steven J Siegel1, Aoife M Roche1, Jeffrey N Weiser2

  • 1Department of Microbiology, University of Pennsylvania, Philadelphia, PA 19104, USA.

Cell Host & Microbe
|July 11, 2014
PubMed

Insights

Influenza infection boosts Streptococcus pneumoniae growth by increasing sialic acid availability in airways, worsening secondary pneumonia. This suggests targeting sialic acid could combat coinfection severity.

Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Secondary bacterial pneumonia, especially from Streptococcus pneumoniae, significantly contributes to influenza-associated mortality.
  • The precise mechanisms driving influenza and Streptococcus pneumoniae coinfection remain incompletely understood.

Purpose of the Study:

  • To elucidate the mechanisms by which influenza virus infection enhances Streptococcus pneumoniae colonization and subsequent pneumonia.
  • To identify host-derived factors that promote bacterial proliferation during coinfection.

Main Methods:

  • Murine models of influenza and Streptococcus pneumoniae coinfection.
  • Analysis of bacterial colonization, replication, and lung spread.
  • Metabolomic analysis of airway secretions.
  • Genetic manipulation of Streptococcus pneumoniae and host genes (Muc5ac).
  • Assessment of mucolytic treatment effects.

Main Results:

  • Prior influenza infection significantly enhances pneumococcal colonization and promotes bacterial spread to the lungs in mice.
  • Influenza infection increases the availability of sialic acid, a host metabolite, which stimulates pneumococcal proliferation.
  • Pneumococcal sialic acid catabolism genes are essential for influenza to promote bacterial growth.
  • Reducing sialic acid availability, via genetic deletion of Muc5ac or mucolytic treatment, limits influenza-induced pneumococcal replication.

Conclusions:

  • Influenza virus infection creates a favorable environment for Streptococcus pneumoniae by increasing sialic acid availability.
  • This increased sialic acid promotes pneumococcal proliferation, colonization, and aspiration, contributing to severe coinfection.
  • Targeting sialic acid metabolism or availability presents a potential therapeutic strategy against influenza-bacterial coinfections.

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