Interleukin-1 Release by Alveolar Macrophages in Asthmatic Patients and Healthy Subjects

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Abstract
A thymocyte proliferative response assay was used to compare spontaneous and lipopolysaccharide (LPS)-induced interleukin-1 (IL-1) release by alveolar macrophage (AM) in asthmatic patients and normal subjects. Twelve asthmatic patients and seven nonsmoking healthy subjects underwent a bronchoalveolar lavage (BAL). All asthmatic patients had a reversible airway obstruction and 7/12 were allergic. BAL AM were separated by adherence on tissue culture plates in medium RPMI-1640 supplemented with antibiotics and fetal calf serum, and were incubated with or without 10 μg/ml LPS for 20 h. Free-cell supernatants were tested by C3H/HeJ mice thymocyte proliferative assay. Unstimulated AM supernatant IL-1 activity was significantly higher in asthmatic patients (mean ± SEM: 47.8 ± 11.9 units/106 AM) in comparison with healthy subjects (4.8 ± 2.3 units/106 AM; p < 0.05, Mann-Whitney U test) but did not significantly differ between allergic (42.2 ± 15.5 units/106 AM) and intrinsic asthmatic patients (55.8 ± 20.7 units/106 AM). For healthy subjects, IL-1 activity was significantly higher in LPS-stimulated AM supernatants (85 ± 20 units/106 AM, p < 0.05; Mann-Whitney U test) in comparison with unstimulated ones; for asthmatic patients, unstimulated and LPS-stimulated AM supernatant IL-1 activity did not significantly differ. This finding is in accordance with previous work suggesting that AM from asthmatic patients have a weak suppressive activity upon lymphocyte proliferation and emphasize the enhanced AM releasability in asthma.