Aerts C, Wallaert B, Grosbois J M, Voisin C
Ann N Y Acad Sci. 1986;465:193-200. doi: 10.1111/j.1749-6632.1986.tb18495.x.
Biological mechanisms involving nonprotease factors mediate the alterations of the alveolar structures which lead to the interstitial fibrosis of pulmonary sarcoidosis. Thus, we have investigated the production of oxidant species by BAL cells from 50 sarcoidosis patients and 18 healthy controls using a lucigenin-dependent CL method. Spontaneous and PMA-induced CL's were significantly higher in untreated patients and treated patients than in spontaneously cured patients or healthy controls (p less than .05). SOD inhibits 60 to 75% of spontaneous CL and 91 to 93% of PMA-induced CL. There was no apparent correlation between the CL of AM's and the radiological types, SACE levels, and gallium scans. In marked contrast, CL was significantly higher in patients with increased alveolar lymphocytosis (greater than or equal to 18%) than in patients with normal BAL. Since there were neither neutrophils nor eosinophils in BAL and since lymphocytes do not produce lucigenin-dependent CL, we believe that CL is produced by AM's. CL inhibition by SOD suggests that superoxide anion is involved in the production of CL. The release of both superoxide anion and related radicals may be of importance in the pathogenesis of pulmonary sarcoidosis.
涉及非蛋白酶因子的生物学机制介导了肺泡结构的改变，进而导致肺结节病的间质纤维化。因此，我们采用基于光泽精的化学发光法，研究了50例结节病患者和18名健康对照者支气管肺泡灌洗（BAL）细胞产生氧化剂的情况。未经治疗的患者和已治疗的患者中，自发的和佛波酯（PMA）诱导的化学发光均显著高于自发治愈的患者或健康对照者（p < 0.05）。超氧化物歧化酶（SOD）可抑制60%至75%的自发化学发光以及91%至93%的PMA诱导的化学发光。肺泡巨噬细胞（AM）的化学发光与放射学类型、血清血管紧张素转换酶（SACE）水平及镓扫描之间无明显相关性。与之形成显著对比的是，肺泡淋巴细胞增多（≥18%）的患者的化学发光显著高于BAL正常的患者。由于BAL中既无中性粒细胞也无嗜酸性粒细胞，且淋巴细胞不产生基于光泽精的化学发光，我们认为化学发光是由AM产生的。SOD对化学发光的抑制表明超氧阴离子参与了化学发光的产生。超氧阴离子及相关自由基的释放可能在肺结节病的发病机制中具有重要作用。
