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Influenza A virus accelerates neutrophil apoptosis and markedly potentiates apoptotic effects of bacteria
M L Colamussi1, M R White, E Crouch
1Department of Medicine and Pathology, Boston University School of Medicine, Boston, MA 02118, USA.
Abstract:
Neutrophils are recruited into the airway in the early phase of uncomplicated influenza A virus (IAV) infection and during the bacterial superinfections that are a significant cause of morbidity and mortality in IAV-infected subjects. In this report, we show that IAV accelerates neutrophil apoptosis. Unopsonized Escherichia coli had similar effects, although apoptotic effects of opsonized E coli were greater. When neutrophils were treated with both IAV and unopsonized E coli, a marked enhancement of the rate and extent of neutrophil apoptosis occurred as compared with that caused by either pathogen alone. Treatment of neutrophils with IAV markedly increased phagocytosis of E coli. Simultaneous treatment of neutrophils with IAV and E coli also elicited greater hydrogen peroxide production than did either pathogen alone. IAV increased neutrophil expression of Fas antigen and Fas ligand, and it also increased release of Fas ligand into the cell supernatant. These findings may have relevance to the understanding of inflammatory responses to IAV in vivo and of bacterial superinfection of IAV-infected subjects.
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.