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Tumor necrosis factor-alpha (TNF-alpha) is an important proinflammatory cytokine. Recently, pentoxifylline (POF) has been shown to suppress the synthesis of TNF-alpha from lipopolysaccharide (LPS)-stimulated human monocytes in cell cultures and in vivo. The aim of this study was to investigate whether POF-induced suppression of TNF-alpha secretion affects peripheral blood monocytes (PBM) and alveolar macrophages (AM) equally, and whether POF is able to suppress the spontaneous TNF-alpha production from AM in pulmonary sarcoidosis in vitro. In seven patients without interstitial lung disease we studied the effect of POF on LPS-stimulated PBM and AM cultured for 24 h. In six patients with sarcoidosis we investigated the effect of POF on the enhanced spontaneous TNF-alpha production by AM in vitro. POF induced a dose-dependent suppression of the LPS-stimulated TNF-alpha production which was not different for PBM and AM, respectively. In sarcoidosis, POF inhibited the spontaneous TNF-alpha production of AM at 0.1 mM by 91% and at 1 mM by 98%. In conclusion, POF inhibits LPS-induced TNF-alpha production from PBM and AM to a similar extent and can also inhibit the exaggerated spontaneous TNF-alpha production from AM in sarcoidosis in vitro. This may be the basis for further clinical trials to evaluate POF as an immunotherapeutic agent in sarcoidosis.

A structural phase transformation in the CuO 2 planes of YBa 2 Cu 3 O x has been observed at the onset of the overdoped regime, x 6.95. We have measured as a function of x the dimpling in the CuO 2 planes by EXAFS, and the O(2,3) in-phase ͑A 1g ͒ mode by Raman scattering. The data show for x $ 6.95 anomalously large static displacements of the Cu (2) atoms off the O(2,3) layer and a gap in the distribution of the O(2,3) in-phase Raman shifts. We conclude the structure of overdoped YBa 2 Cu 3 O x to be a martensitic form of the optimum doped crystal. [S0031-9007(97)04809-6]

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