Neutrophils as Effectors of Host Defense and Host Damage. Physiopathology and Perspectives of Pharmacological Manipulation

Although neutrophils (neutrophilic polymorphonuclear leukocytes, PMNs) provide a principal means of host defense against bacteria and fungi, they can also promote host tissue injury in several non infectious diseases (1). The intervention of PMNs in the pathogenesis of gouty arthritis, rheumatoid arthritis, autoantibody -and immunecomplex-mediated glomerulo-nephritis has been well documented. Moreover, a relevant role of PMNs in tissue injury is now more than suggestive in an increasing number of disease states, including immune vasculitis, ulcerative colitis, chronic obstructive pulmonary disease, adult acute respiratory distress syndrome. At present, the same toxic potential of PMNs is generally thought to be equally responsible for both the microorganism killing and the tissue injury in the aforementioned disorders (1, 2, 3). This fact, coupled with the incomplete knowledge of the events underlying the PMN responses and the PMN-mediated tissue injury, makes rational therapeutic approaches untimely at least as far as the dangerous effects of PMNs are concerned.