Specific Proteins of Inflammatory Cells and α1-Proteinase Inhibitor in Alveolar Epithelial Lining Fluid of Polytraumatized Patients: Do They Indicate Posttraumatic Lung Failure?

Despite numerous hints that activated inflammatory cells may trigger lung injury, the causative role especially of the polymorphonuclear (PMN) granulocytes (neutrophils) to promote enhanced microvascular permeability in acute respiratory distress syndrome (ARDS) is still a matter of debate [22, 25, 27, 28, 31]. In the early 1980s, Hammerschmidt et al. [11] demonstrated that complement-mediated neutrophil sequestration in pulmonary capillaries leading to lung vascular endothelial injury was a common feature of patients suffering from acute respiratory distress syndrome (ARDS). Meanwhile, however, a wealth of basic information exists indicating that neutrophil activation occurs to a similar extent in high-risk patients who do not, however, eventually develop ARDS [21]. Moreover, signs of ARDS have been described in neutropenic patients, thus calling into question whether neutrophils are required in the generation of ARDS [19]. Yet, the latter observations may be taken as an indirect evidence for the importance of other inflammatory cells, e.g., activated alveolar macrophages [7], in disturbing the alveolar barrier from the epithelial side of the alveoli, at least in neutropenic patients.