ABSTRACT
Polymorphonuclear leukocytes (PMN) play determinant roles in immunity and inflammation. These processes are mediated by the activation of the NADPH oxidase, which generates superoxide anion (O2), and by the activation of a cytoplasmic, constitutive and inducible nitric oxide synthase (NOS and iNOS), which produces nitric oxide (NO*) (1-5). Superoxide anion, H2O2, and NO" are not only efficient antimicrobial effector molecules, they are key mediators in inflammatory reactions in which they participate, altering the expression of endothelial adhesion molecules and inducing the production of different cytokines (6-8). Together with these molecules and proteolytic enzymes, PMN cells can mediate intra-and extracellular cytotoxicity and modulate different cellular functions in adjacent cells. After degradation of the ingested material, polymorphonuclear cells die. These terminally differentiated cells are not able to proliferate and in vitro they demise rapidly by an apoptotic mechanism; PMN senecent cells are then recognized by macrophages by a cell-surface mechanism mediated by vitronectin receptor (9).
