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Blood, Vol. 93 No. 7 (April 1), 1999:
pp. 2395-2403
Influenza A Virus Accelerates Neutrophil Apoptosis and Markedly
Potentiates Apoptotic Effects of Bacteria
Maria Luisa Colamussi,
Mitchell R. White,
Erika Crouch, and
Kevan
L. Hartshorn
From the Department of Medicine and Pathology, Boston University
School of Medicine, Boston, MA; and the Department of Pathology, The
Jewish Hospital, Washington University School of Medicine, St Louis,
MO.
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 occured 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.
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