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

Neutrophils are recruited into the airway in the early phase of uncomplicat ed influenza A virus (IAV) infection and during the bacterial superinfectio ns 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 coil had similar effects, although apoptotic effe cts of opsonized E coil were greater. When neutrophils were treated with bo th IAV and unopsonized E coil, a marked enhancement of the rate and extent of neutrophil apoptosis occured as compared with that caused by either path ogen alone. Treatment of neutrophils with IAV markedly increased phagocytos is of E coli. Simultaneous treatment of neutrophils with IAV and E coli als o elicited greater hydrogen peroxide production than did either pathogen al one. IAV increased neutrophil expression of Fas antigen and Fas ligand, and it also increased release of Fas ligand into the cell supernatant. These f indings may have relevance to the understanding of inflammatory responses t o IAV in vivo and of bacterial superinfection of IAV-infected subjects. (C) 1999 by The American Society of Hematology.