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Under normal conditions, the release of interleukin 1 (IL-1) and IL-1 inhibitors play a role in tissue homeostasis. We have already reported an increase in IL-1 activity and a decrease in IL-1 inhibitory activity (IHA) in the supernatants of alveolar macrophages from healthy long-term smokers as compared with healthy nonsmokers. In this study, we report an alteration in the release of IL-1 and IL-1 IHA from alveolar macrophages in patients with interstitial lung diseases (sarcoidosis and idiopathic pulmonary fibrosis [IPF]). IL-1 activity released from alveolar macrophages stimulated by lipopolysaccharide was increased in patients with active sarcoidosis (mean +/- SD, 2.52 +/- 1.33 U/ml [n = 6] vs 1.38 +/- 0.62 U/ml [n = 15] for healthy non-current smokers [HNS]; p less than 0.05). IL-1 IHA released from alveolar macrophages was significantly different among the groups examined: a decrease of IL-1 IHA occurred in patients with active sarcoidosis (61.4 +/- 19.2 [n = 6] vs 85.9 +/- 13.9 percent:HNS; p less than 0.05) and IPF (64.7 +/- 18.5 [n = 9]; p less than 0.05). Prednisolone in the culture medium at physiologic concentrations suppressed the release of IL-1 and enhanced the release of IL-1 IHA. IL-1 IHA inhibited not only mouse thymocyte proliferation but also human fibroblast proliferation in the presence of IL-1.
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