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Neutrophils play a key role in the physiopathogenesis of acute lung injury in general and acute respiratory distress syndrome (ARDS) in particular. To identify the anti-inflammatory mediators with a protective effect on lung tissue damage in ARDS, we correlated the concentration of the Clara cell 16-kD protein (CC16; an inhibitor of neutrophil chemotaxis), angiogenin (an inhibitor of degranulation), and the total radical oxygen neutralizing activity with the amount of elastase (a marker of neutrophil activation) and with the Pao2/Fio2 ratio, which is inversely related to lung injury.University hospital.Patients with ARDS (n = 12) and patients at risk for developing ARDS (n = 14).Patients underwent bronchoalveolar lavage 12 hrs after diagnosis of ARDS or at-risk status.The amount of CC16 and radical oxygen neutralizing activity was not significantly different in patients with or at risk for ARDS. In contrast, the amount (mean ± sem) of angiogenin in the bronchoalveolar lavage of ARDS patients (45 ± 14 ng/mL, n = 12) was increased 11-fold (p < .05) compared with patients at risk for ARDS (4 ± 1 ng/mL, n = 14). In patients with ARDS, the amount of protein and angiogenin in bronchoalveolar lavage increased with decreasing concentration of CC16 (p < .05). In addition, CC16 correlated with the Pao2/Fio2 ratio (p < .05) and inversely with the amount of elastase (p < .05) and thus may be regarded as a reliable protective agent for lung injury.A high concentration of CC16, a natural inhibitor of neutrophil function, decreases neutrophil-mediated lung damage of patients with ARDS. Strategies to increase natural anti-inflammatory agents, and thus influence the disruption of the balance between natural inflammatory and anti-inflammatory or protective factors, could be useful to modulate the tissue destruction and the course of ARDS.