Differential effect of soluble fibrinogen as a neutrophil activator.

A fundamental paradigm involved in acute inflammatory responses to invading pathogens and tissue damage is the migration of specific leukocyte populations to the affected tissues to mount an initial innate response to the aggression. The recruitment of polymorphonuclear neutrophils (PMNs) from the blood is a central event in this respect. The aim of this study was to understand whether fibrinogen is able to modulate the pattern of neutrophil activation and thus contribute to neutrophil recruitment. We demonstrated that fibrinogen induces free radical production by neutrophils without modifying the activation status of Mac-1 (αMβ2, CD11b/CD18), the previously identified neutrophil receptor for fibrinogen. This data indicates that fibrinogen must have an additional different binding site in the neutrophil membrane. Importantly, we propose that as Mac-1 activation was not affected by the binding of fibrinogen, activated neutrophils can further maintain their ability to marginate, roll and adhere to the endothelial walls.