Strausz J, Männel D N, Pfeifer S, Borkowski A, Ferlinz R, Müller-Quernheim J
Third Department of Internal Medicine, Johannes Gutenberg University, Mainz, FRG.
Int Arch Allergy Appl Immunol. 1991;96(1):68-75. doi: 10.1159/000235537.
In pulmonary sarcoidosis an activation of alveolar T lymphocytes and alveolar macrophages (AM) has been demonstrated. There is evidence that in contrast to acute disease a heightened T-cell response cannot be observed in the chronic phase of sarcoidosis. The role of AM in the inflammatory process of chronic sarcoidosis is not yet intensively evaluated. To address this question we measured the release of tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1) by AM of 39 patients with chronic sarcoidosis (duration greater than 4 years; 30 active, 9 inactive diseases) without therapy and correlated the monokine release with parameters of T-cell alveolitis and the course of the disease. The T4/T8 ratio was higher in the active than in the inactive group without reaching statistical significance. TNF alpha as well as IL-1 is spontaneously released by AM of the active group 2,099 +/- 518 pg/ml TNF alpha/10(6) cells/24 h and 8/13 (IL-1+/total) respectively. In the inactive group the AM release 375 +/- 246 pg/ml TNF alpha/10(6) cells/24 h which is in the range of the control and 1 out of 5 patients was IL-1-positive. There was no correlation between the monokine release and any parameter of T-cell alveolitis. These data support the hypothesis that the inflammatory process in chronic sarcoidosis is dominated by the activity of AM and that this activity determines the course of the disease.
在肺结节病中,已证实肺泡T淋巴细胞和肺泡巨噬细胞(AM)被激活。有证据表明,与急性疾病相反,在结节病的慢性期未观察到T细胞反应增强。AM在慢性结节病炎症过程中的作用尚未得到深入评估。为了解决这个问题,我们测量了39例未经治疗的慢性结节病患者(病程大于4年;30例活动期,9例非活动期疾病)的AM释放肿瘤坏死因子α(TNFα)和白细胞介素-1(IL-1)的情况,并将单核因子释放与T细胞肺泡炎参数及疾病进程相关联。活动组的T4/T8比值高于非活动组,但未达到统计学意义。活动组的AM可自发释放TNFα以及IL-1,分别为2,099±518 pg/ml TNFα/10⁶细胞/24小时和8/13(IL-1⁺/总数)。在非活动组中,AM释放375±246 pg/ml TNFα/10⁶细胞/24小时,处于对照范围内,5例患者中有1例IL-1呈阳性。单核因子释放与T细胞肺泡炎的任何参数之间均无相关性。这些数据支持以下假设:慢性结节病中的炎症过程以AM的活性为主导,并且这种活性决定了疾病的进程。