Polymorphonuclear neutrophil leukocytes are major cellular contributors in the process of inflammation in response to infections. These cells represent one of the first lines of defence against microbial invasion. Influx of neutrophils into inflammatory sites results in phagocytosis, killing and removal of pathogenic micro-organisms, and can also participate in healing and tissue repair (Smolen and Boxer, 1995). However, uncontrolled accumulation of neutrophils, and inadequate responses of these cells can initiate acute or chronic inflammatory disorders (Smith, 1994). One of the first steps in the inflammatory process is the release of various substances from host cells as well as from the pathogens, which will then attract and activate circulating neutrophils. Such chemoattractants include N-formylated peptides derived from bacterial walls, the complement-derived C5a, membrane lipid metabolites, and the more recently described chemokines (Sandborg and Smolen, 1988; Schall and Bacon, 1994). Chemotaxis implies that neutrophils will have to cross cellular barriers such as the vascular endothelium and possibly various epithelia, and to progress through connective tissues and extracellular matrices (Nourshargh and Williams, 1995). Major metabolic events then occur to initiate phagocytosis when neutrophils contact the offending organism. During phagocytosis, different harmful substances aimed at destroying the pathogens and which are normally restricted to internal phagolysosomes, can also be exteriorized. Then, they affect the host cells and extracellular matrices, contributing to tissue damage. The releasable granule products include lysosomal hydrolases, myeloperoxidase and serine proteinases. Cytotoxic agents are also formed from the plasma membrane, i.e. highly reactive oxygen metabolites such as the superoxide anion , hydrogen peroxide (H2O2), and hydroxyl radical and its chlorinated derivatives (Witko-Sarsat and Descamps-Latscha, 1994). Three other types of neutrophil-derived mediators, although noncytotoxic by themselves, participate to and can amplify the inflammatory process, namely the platelet-activating factor (PAF), chemokines, and arachidonate metabolites known as eicosanoids.