Neutrophil activation for adherent and nonadherent cells, as measured by fl
ow cytometry, was not strongly dependent on material surface chemistry. We
had hypothesized that material-induced neutrophil activation was an importa
nt parameter associated with material failure. All materials tested [cellop
hane, an acrylonitrile copolymer (AN69), Pellethane(TM) nylon, polyethylene
terephthalate, low density polyethylene, and polydimethylsiloxane] activat
ed isolated human neutrophils, which were resuspended in plasma or serum, t
o similar extents based on L-selectin shedding, CD11b upregulation, and sti
mulation of the oxidative burst after 30-min exposure. Inhibition of comple
ment activation by sCR1 unexpectedly had Little effect if any on nonadheren
t neutrophils. However, neutrophil adhesion, but not the level of activatio
n of the adherent cells, was strongly dependent on complement activation. P
retreatment with albumin did not inhibit adhesion or reduce neutrophil acti
vation, but plasma pretreatment resulted in increased activation for nonadh
erent and adherent cells. More adhesion and a higher level of activation of
adherent cells was observed following pretreatment with fibrinogen, a liga
nd of CD11b. Taken together these results suggest that upon contact with a
material, neutrophil activation may occur though mechanisms that are not me
diated by complement. For example, the presence of plasma proteins such as
fibrinogen at the interface may trigger activation and the release of other
activating agents. Although the material differences are small, the extent
of activation may be significant and warrant further study of the mechanis
m and consequences of that activation. (C) 1999 John Wiley & Sons, Inc.