Immune interferon is a growth factor for human lung fibroblasts.

A number of immunologically mediated lung disorders are characterized by the presence of fibrosis. In these studies, we demonstrate that immune (gamma) interferon, as well as interleukin-1 (IL-1), can function as a growth factor for human lung fibroblasts. Interleukin-2 has no effect on the proliferation of these cells.

Augmentation of fibroblast proliferation by bleomycin.

Bleomycin-induced lung disease is characterized by fibroblast proliferation and pulmonary fibrosis. In these studies, we demonstrate that fibroblasts are relatively resistant to clinically relevant amounts (below 10(-4) U/ml) of bleomycin and that these levels of bleomycin augment fibroblast proliferation in response to various fibroblast growth factors. These observations suggest that one mechanism by which bleomycin causes pulmonary fibrosis is augmentation of fibroblast proliferation.

Interferon and growth factor activity for human lung fibroblasts. Release from bronchoalveolar cells from patients with active sarcoidosis.

Pulmonary sarcoidosis is a granulomatous disorder of unknown etiology characterized by both an active cellular immune process and interstitial fibrosis. It has recently been demonstrated that gamma-interferon (the type of interferon associated with an active cellular immune process) is also a potent growth factor for human lung fibroblasts. To evaluate the hypothesis that there is an association between the release of immune interferon and the release of growth factor activity for fibroblasts, bronchoalveolar cells from patients with sarcoidosis were studied for the spontaneous release of both immune interferon and growth factor activity for fibroblasts.