[Pentoxifylline inhibits secretion of O2- and TNF-alpha by alveolar macrophages in patients with sarcoidosis].

Immunitat und Infektion Pub Date : 1995-06-01

M Körber, S Kamp, H Kothe, J Braun, K Dalhoff

引用次数: 0

Abstract

Reactive oxygen species (ROS) and cytokines like tumor necrosis factor-alpha (TNF-alpha) play a crucial role as inflammatory mediators in pulmonary sarcoidosis. We examined the antiinflammatory effect of pentoxifylline (POF) on alveolar macrophages (AM) of patients with sarcoidosis in vitro. We could demonstrate that POF (above 4.10(-4) M) inhibited the secretion of superoxide anion and TNF-alpha by AM in a dose-dependent manner via a prostaglandin synthesis-dependent mechanism that was independent of the glucocorticoid receptor. POF is an interesting immunomodulating substance that should be further evaluated in clinical trials.

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[己酮可可碱抑制结节病患者肺泡巨噬细胞分泌O2-和tnf - α]。

活性氧(ROS)和细胞因子如肿瘤坏死因子- α (tnf - α)在肺结节病中作为炎症介质起着至关重要的作用。我们在体外研究了己酮可可碱(POF)对结节病患者肺泡巨噬细胞(AM)的抗炎作用。我们可以证明，POF(高于4.10(-4)M)通过不依赖糖皮质激素受体的前列腺素合成依赖机制，以剂量依赖的方式抑制AM分泌超氧阴离子和tnf - α。POF是一种有趣的免疫调节物质，值得在临床试验中进一步评估。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Immunitat und Infektion

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