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Mediators of Inflammation
Volume 1 (1992), Issue 5, Pages 319-322

Suppressive effect of TNF-α and IL-1 on alveolar fibroblast proliferation in sarcoidosis

1Department of Pulmonary Diseases and Allergic Diseases, TeI-Aviv Medical Center, Ichilov Hospital, 6 Weizmann Street, TeI-Aviv 64268, Israel
2Department of Internal Medicine “T”, Ichilov Hospital, 6 Weizmann Street, TeI-Aviv 64239, Israel
3Department of Human Microbiology, Sackler School of Medicine, TeI-Aviv University, Ramat Aviv, TeI-Aviv 69978, Israel
4Department of Virology, Weizmann Institute of Science, Rehovot 76326, Israel

Copyright © 1992 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The nature of soluble factors that regulate fibroblast proliferation have not been finally characterized. Our aim was to study the role of tumour necrosis factor α (TNF-α) and interleukin-1 (IL-1) in the suppressive activity of alveolar macrophages on autologous lung fibroblasts proliferation in sarcoidosis. We found that supernatants recovered from alveolar macrophages suppressed the proliferation of alveolar fibroblast in sarcoidosis by 35.5 ± 1.13% compared to 3 ± 16% in controls (p < 0.001 between the two groups). This suppression correlated with high content of TNF-α and IL-1 in sarcoidosis patients stage II-III (7.7 ± 2.9 ng/ml TNF-α and 157 ± 53 U/ml IL-1 compared to 3.4 ± 2.4 ng/ml TNF-α and 43 U/ml IL-1 in controls; p < 0.01 and p < 0.001, respectively). Both cytokines in sarcoidosis stage I were within the normal ranges. Exogenous TNF-α (1000-0.5 ng/ml) and IL-1 (500-0.24 ng/ml) had an additive suppressive activity on fibroblast proliferation which was partially reversed by indomethacin.