Fibroblasts play a crucial role in :progressive lung fibrosis, acting
not only as target cells but also as effector cells. To clarify these
functions in sarcoidosis, lung fibroblasts from Japanese sarcoid patie
nts were studied for their proliferative capacity and cytokine product
ivity. Fibroblasts were cultured from transbronchial lung biopsy speci
mens from seven patients with sarcoidosis. As a comparison, fibroblast
s from open lung biopsy specimens of four patients with idiopathic pul
monary fibrosis (IPF) were studied. For controls, fibroblasts were cul
tured from specimens of normal resected lung tissue of five patients w
ith localized lung cancer. The proliferative activity of cultured fibr
oblasts from patients with sarcoidosis was highest among the three gro
ups (p < 0.05). However. the proliferative capacity in all groups was
suppressed when fibroblasts were cultured with interleukin-1 beta (IL-
1 beta). No significant differences were noted in the degree of inhibi
tion among the three groups. Addition of interferon-gamma (IFN-gamma)
also resulted in inhibition of fibroblast growth in all groups, but th
e degree of inhibition was significantly greater in both the sarcoid a
nd IPF groups than in controls (p < 0.05). The amount of interleukin-6
(IL-6) in the culture supernatants from sarcoid fibroblasts coculture
d with IL-1 beta was significantly higher than in controls. Sarcoid fi
broblasts are not only proliferatively active but also possess effecto
r cell function to produce cytokines. IL-6 may enhance the immunologic
reaction to sarcoidosis and cause the disease to become chronic. IFN-
gamma suppresses proliferation of sarcoid fibroblasts and may prevent
fibrotic changes of the lungs in che Japanese sarcoid patients.