Role of interleukin 8 in the genesis of acute respiratory distress syndrome through an effect on neutrophil apoptosis.

Abstract
THE ACUTE respiratory distress syndrome (ARDS) appears to be an inflammatory process in which activated neutrophils (PMNs) may play a role. There is evidence to suggest that PMNs may influence or initiate injury to the pulmonary alveolar-capillary membranes, leading to flooding of the alveolar spaces, disruption of normal gas exchange, and severe, refractory hypoxemia.1 Large numbers of PMNs accumulate within the lung in the early phase of ARDS, such that PMNs constitute 80% or more of the total cells obtained by bronchoalveolar lavage (BAL), compared with approximately 3% in normal subjects. Stimulation of PMNs to secrete elastase, myeloperoxidase, and toxic oxygen metabolites leads to the observed lung injury.1