The role of polymorphonuclear leukocytes in the pathogenesis of the adult respiratory distress syndrome

Polymorphonuclear leukocytes (PMNL) constitute the first line of defence in the protection of the host from invading microorganisms. PMNL also contribute to the removal of cellular debris from necrotic tissues during reparative processes. For these purposes PMNL are armed with highly efficient bactericidal mechanisms which, under certain pathophysiological conditions, can be turned against the host himself. A vast body of evidence indicates that PMNL are able to cause lung injury which may be followed by the development of acute respiratory distress syndrome (ARDS). Accordingly, in patients with ARDS blood concentrations of inflammatory activators of PMNL are elevated, cytotoxic mechanisms of PMNL are enhanced and sequestration of these cells has been demonstrated to be inversely proportional to gas exchange. The manifestation of ARDS in leukopenic patients, however, indicates the development of this clinical syndrome independently of the presence of PMNL. The ability to differentiate between PMNL-dependent and PMNL-independent pathways in the pathogenesis of this syndrome is not only of theoretical interest but also of therapeutic significance. Since the patient's systemic inflammatory response may vary according to the stage and type of the underlying disease, an exact qualitative and quantitative analysis of PMNL functions may provide the rationale for new anti-inflammatory drug regimens aimed at modifying the host's response without increasing the risk of infection.