Influenza A virus accelerates neutrophil apoptosis and markedly potentiates apoptotic effects of bacteria

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Published on: January 20, 2017

M L Colamussi1, M R White, E Crouch

  • 1Department of Medicine and Pathology, Boston University School of Medicine, Boston, MA 02118, USA.

Blood
|March 26, 1999
PubMed

Insights

Influenza A virus (IAV) and bacteria accelerate neutrophil apoptosis. Combined IAV and E. coli infection significantly enhances neutrophil apoptosis, phagocytosis, and hydrogen peroxide production, impacting immune responses.

Area of Science:

  • Immunology
  • Virology
  • Microbiology

Background:

  • Neutrophils are crucial in airway inflammation during influenza A virus (IAV) infection.
  • Bacterial superinfections significantly increase morbidity and mortality in IAV-infected individuals.

Purpose of the Study:

  • To investigate the effects of IAV and Escherichia coli (E. coli) on neutrophil apoptosis.
  • To explore the combined impact of IAV and E. coli on neutrophil function.

Main Methods:

  • Neutrophils were treated with IAV, unopsonized E. coli, and opsonized E. coli.
  • Combined treatments of IAV and E. coli were analyzed for apoptosis, phagocytosis, and hydrogen peroxide production.
  • Neutrophil expression and release of Fas antigen and Fas ligand were assessed.

Main Results:

  • IAV accelerates neutrophil apoptosis; E. coli also induces apoptosis, with greater effects from opsonized bacteria.
  • Co-treatment with IAV and unopsonized E. coli markedly enhanced neutrophil apoptosis, phagocytosis, and hydrogen peroxide production.
  • IAV increased neutrophil Fas antigen and Fas ligand expression and release.

Conclusions:

  • IAV and bacterial coinfection synergistically promote neutrophil apoptosis, potentially influencing inflammatory responses.
  • Findings provide insights into the mechanisms underlying severe outcomes of secondary bacterial infections post-influenza.
  • Understanding these interactions is vital for managing IAV-associated complications.

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