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Capillary leakage provides nutrients and antioxidants for rapid pneumococcal proliferation in influenza-infected

Vicky Sender1, Karina Hentrich1, Anuj Pathak1

  • 1Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-17177 Stockholm, Sweden.

Proceedings of the National Academy of Sciences of the United States of America
|November 24, 2020
PubMed

Insights

Secondary bacterial infections, like those caused by pneumococci, worsen influenza A virus (IAV) outcomes. This study reveals how IAV alters lung environments, promoting bacterial growth and survival through nutrient availability and bacterial adaptation.

Area of Science:

  • Microbiology
  • Immunology
  • Respiratory Medicine

Background:

  • Influenza A virus (IAV) infection often leads to mortality due to secondary bacterial pneumonia, particularly by Streptococcus pneumoniae.
  • Understanding the host-pathogen interactions during coinfection is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate how IAV infection alters the lung environment and influences pneumococcal replication in the lower respiratory tract (LRT).
  • To identify bacterial factors and host-derived molecules that facilitate pneumococcal survival and growth during IAV coinfection.

Main Methods:

  • Coinfection model in mice with Influenza A virus and Streptococcus pneumoniae.
  • Bronchoalveolar lavage (BAL) fluid analysis.
  • Metabolomic and quantitative proteomic analyses.
  • In vitro growth assays with varying conditions and bacterial mutant strains.

Main Results:

  • IAV infection caused rapid pneumococcal proliferation in the LRT within 4-6 hours.
  • Metabolomic and proteomic data indicated capillary leakage, leading to nutrient and antioxidant efflux into the alveolar space.
  • Pneumococci upregulated the chaperone/protease HtrA in response to IAV-induced inflammation and oxidative stress.
  • HtrA conferred a growth advantage in the IAV-infected LRT and protected against complement-mediated opsonophagocytosis via enhanced capsular production.
  • Absence of HtrA resulted in bacterial growth arrest, partially rescued by antioxidants.

Conclusions:

  • Pneumococcal growth in IAV-infected lungs is supported by a nutrient-rich environment with elevated antioxidants like ascorbic acid.
  • Bacterial adaptation, including HtrA expression and enhanced capsule production, is critical for coping with oxidative damage and immune clearance.
  • Targeting bacterial adaptation mechanisms may offer novel therapeutic strategies against secondary bacterial pneumonias following influenza.
Keywords:
Streptococcus pneumoniaeantioxidantsinfluenza A viruspneumococciredox imbalance

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