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*
División Inmunología and
División Medicina Experimental, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina
The acute phase of the inflammatory response involves an increase
in the concentrations of different plasma proteins that include
fibrinogen (Fbg) and multiple proinflammatory mediators. In parallel,
neutrophil activation is thought to play a crucial role in several
inflammatory conditions, and it has been recently demonstrated that Fbg
specifically binds to the 
-subunit of CD11b/CD18 on neutrophil
surface. Although several reports have shown that CD11b engagement
modulates neutrophil responses, the effect of human Fbg (hFbg), one of
CD11b physiologic ligands, has not been exhaustively investigated. We
have now shown that incubation of purified neutrophils with hFbg
induces a transient and rapid elevation of free intracellular
Ca2+. This early intracellular signal is accompanied by
changes in the expression of neutrophil activation markers, including
enhancement of CD11b and CD66b, and down-regulation of Fc
RIII. In
addition, we have evaluated the effect of hFbg on two functional events
related to expression and resolution of inflammation: cytotoxic
capacity and rate of neutrophil apoptosis. We have found that
activation of neutrophils by hFbg resulted in both enhancement of
phagocytosis and Ab-dependent cellular cytotoxicity, and delay of
apoptosis. We conclude that during inflammatory processes, soluble Fbg
could influence neutrophil responses, increasing and prolonging their
functional capacity.
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