Role of the sialophorin (CD43) receptor in mediating influenza A virus-
induced polymorphonuclear leukocyte dysfunction
JS Abramson and HR Hudnor
Department of Pediatrics, Bowman Gray School of Medicine of Wake Forest
University, Winston-Salem, NC 27157.
Polymorphonuclear leukocytes (PMNLs) exposed to influenza A virus (IAV)
undergo activation of the respiratory burst followed by depression of cell
function when subsequently exposed to particulate or soluble stimuli. The
effect of IAV on PMNLs is likely to be mediated through the attachment of
IAV to one or more specific receptors. Recently, IAV has been shown to bind
to the sialophorin protein (CD43) receptor on PMNL plasma membranes. The
present study was performed to determine if the sialophorin receptor was
responsible for IAV-induced PMNL dysfunction. When PMNLs were incubated
with IAV or CD43 monoclonal antibody (MoAb) for 30 minutes and then exposed
to a secondary particulate (opsonized zymosan) or soluble (FMLP or phorbol
12- myristate 13-acetate) stimulus, there was significant depression of the
PMNL chemiluminescence response compared with the equivalent control (P
< .05). When PMNL were incubated with the CD43 MoAb and then cross-
linked with a goat antimouse IgG antibody, no depression of PMNL function
occurred upon secondary stimulation. Exposure of cells to IAV aggregates
also eliminated the PMNL dysfunction that normally occurs due to the virus.
Similar to IAV, PMNL dysfunction due to the CD43 MoAb could be overcome by
priming the cells with granulocyte-macrophage colony-stimulating factor.
These findings indicate that IAV-induced PMNL dysfunction is mediated, at
least in part, through the sialophorin receptor.
Volume 85,
Issue 6,
pp. 1615-1619,
03/15/1995
Copyright © 1995 by The American Society of Hematology
