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Mediators of Inflammation
Volume 3, Issue 6, Pages 445-452
http://dx.doi.org/10.1155/S0962935194000633

Differential Proliferative Characteristics of Alveolar Fibroblasts in Interstitial Lung Diseases: Regulative Role of IL-1 and PGE2

1Departments of Pulmonary and Allergic Diseases, Ichilov Hospital, 6 Weizmann Street, Tel-Aviv 64239, Israel
2Department of Human Microbiology, Sackler Faculty of Medicine, Tel-Aviv University, Israel
3Clinical Chemistry, Ichilov Hospital, Tel-Aviv Sourasky Medical Center, Israel
4Internal Medicine “H”, Ichilov Hospital, Tel-Aviv Sourasky Medical Center, Israel
5Department of Thoracic Surgery, Shiba Medical Centre, Israel
6Department of Microbiology and Immunology, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer-Sheva, Israel

Copyright © 1994 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.

Abstract

Fibroblasts (Fb) from patients with sarcoidosis (SA) and hypersensitivity pneumonitis (HP) exhibited a lower proliferative capacity compared with Fb obtained from control (CO) and diffuse interstitial fibrosis patients (DIF). Proliferation of Fb from SA or lip patients was suppressed by autologous LPS-stimulated alveolar macrophages (AM) supernatants but not by those from CO patients. Similarly, alveolar macrophages (AM) derived supernatant, obtained from CO, did not suppress the proliferation of SA and HP Fb. AM from SA and HP patients secreted higher amounts of IL-1α and β compared with controls and compared with Fb from SA and HP patients. Steady levels of IL-1α and βmRNA were expressed in unstimulated and stimulated cultures. Fb from SA and HP patients could be stimulated by LPS to secrete significantly higher levels of PGE2 than those detected in supernatants from LPS stimulated Fb of DIF patients. Only the proliferation of Fb from SA and HP patients was sensitive to amounts of IL-1 equivalent to those detected in the lung of these diseases. As SA and HP are two diseases where irreversible deterioration occurs in only 20% of the patients, we hypothesize that mediators in the lung may modulate Fb proliferation. IL-1 of AM origin and PGE2 of Fb origin secreted at high levels, may be candidates for this suppression because it was abrogated by anti IL-1β and indomethacin.