• T M Siler, J E Swierkosz, T M Hyers, A A Fowler, and R O Webster.
• Department of Internal Medicine, St. Louis University School of Medicine, Missouri 63110.
• Exp. Lung Res. 1989 Dec 1; 15 (6): 881-94.

AbstractThe adult respiratory distress syndrome (ARDS) is characterized by increased neutrophils and macrophages in bronchoalveolar lavage (BAL) fluid. Interleukin-1 (IL-1), an inflammatory mediator produced by macrophages, has been shown to be chemotactic for neutrophils and to stimulate lymphocyte activation and proliferation of fibroblasts. BAL was performed in patients with ARDS, patients at high risk to develop ARDS, and in normal nonsmokers. After removal of cells and surfactant-complexed lipids by centrifugation, the remaining supernatant was concentrated by ultrafiltration utilizing membranes retaining substances greater than 5000 daltons. The concentrate was assayed for immunoreactive IL-1 beta by a radioimmunoassay method. Patients with ARDS (n = 9) had an IL-1 level of 184 +/- 67 pg/ml, high-risk patients (n = 9) had 172 +/- 62 pg/ml, and normals (n = 10) had 4 +/- 1 pg/ml. There was a significant (p less than or equal to .05) increase in IL-1 in the ARDS and risk groups compared to normals. IL-1 was detected in serum from patients with ARDS (n = 19), high risk (n = 19), and normals (n = 8), but no difference was noted among the three groups. BAL cell differentials revealed that neutrophils were increased (p less than .05) in both the ARDS (59 +/- 10%) and high-risk (65 +/- 8%) groups compared to normals (2 +/- 1%). There was a correlation (r = 0.64, p less than .001) between IL-1 levels and BAL protein concentration. BAL IL-1 levels were highest in patients with the fully developed syndrome but were also elevated in patients at high risk. The absence of significant amounts of IL-1 in serum suggests that it may be produced within the lung.

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