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Characterization of influenza A virus activation of the human neutrophil
KL Hartshorn, M Collamer, MR White, JH Schwartz and AI Tauber
William B. Castle Research Hematology Laboratory, Boston City Hospital, MA
02118.
Neutrophil dysfunction consequent to influenza A virus infection has been
described in vivo and in vitro and may contribute to the serious bacterial
sequelae which occur in influenza-infected hosts. On the premise that such
dysfunction may represent a form of "deactivation," we sought to
characterize neutrophil activation by the virus in comparison with other
agonists. The virus induces a respiratory burst in which H2O2 (but not O2-)
are formed. Preceding the respiratory burst, a rise in intracellular
calcium (Ca2+i) is noted, but both responses are nearly independent of
extracellular Ca2+, unlike those elicited by the other well-characterized
Ca2+-dependent agonists, formyl-methyl-leucyl-phenylalanine (FMLP), or
Concanavalin-A (Con-A). The Ca2+ increase is paralleled by IP3 generation,
implying that it is the result of phospholipase C (PLC) activation. The
virus also elicits neutrophil membrane depolarization, which is
independently mediated from the Ca2+ increase and respiratory burst and may
reflect protein kinase C (PK-C) activation. Virus-induced responses are
insensitive to pertussis toxin (PT); cholera toxin does inhibit these
responses but in a nonspecific manner. Thus, although influenza virus
activates PLC in neutrophils, it does so in a PT-insensitive manner and
does not elicit or require a discernible Ca2+ influx to generate a
respiratory burst response. In aggregate, the data indicate that influenza
A virus activates neutrophils in a manner distinct from that of other well-
described neutrophil agonists. These results illustrate the diversity of
neutrophil activation mechanisms and support the notion that further
characterization of this pathway may facilitate understanding of neutrophil
dysfunction induced by the virus.
Volume 75,
Issue 1,
pp. 218-226,
01/01/1990
Copyright © 1990 by The American Society of Hematology
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