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We have recently demonstrated that transforming growth factor beta-2 (TGF-β2) can produce effective pleurodesis. Whether this effect can be reproduced by the use of its downstream proteins is not known. This study compared the effectiveness of TGF-β2 and fibronectin in inducing pleurodesis in rabbits.New Zealand white rabbits (1.5–2.0 kg) were given 1.7 μg of TGF-β2 (n = 5) or 2.0 mg of cellular fibronectin (n = 4) intrapleurally via a chest tube. The induced pleural fluid was collected and analyzed. The rabbits were sacrificed after 14 days. The pleurodesis was graded macroscopically from 1 (none) to 8 (symphysis > 50%).All rabbits in the TGF-β2 group developed effective pleurodesis while none in the fibronectin group had scores > 2 (pleurodesis scores 7.0 ± 0.6 vs 1.3 ± 0.3, P < 0.001). Rabbits that received TGF-β2 produced large amounts of pleural fluid initially (< 4 days). Microscopically, the pleura of rabbits in the TGF-β2 group showed prominent spindle cell proliferation and collagen deposition, but no significant inflammation or mesothelial proliferation. Pleural tissues of rabbits in the fibronectin group had occasional thin collagen deposits only. The intrapleural administration of 2.0 mg of fibronectin, a downstream product of TGF-β, did not induce effective pleurodesis, as did the intrapleural administration of TGF-β2.The present study suggests that the mechanism by which TGF-β2 induces pleurodesis is not predominantly dependent on the production of fibronectin.