Yasuda N, Gotoh K, Minatoguchi S, Asano K, Nishigaki K, Nomura M, Ohno A, Watanabe M, Sano H, Kumada H, Sawa T, Fujiwara H
Second Department of Internal Medicine, Gifu University School of Medicine, Japan.
Respir Med. 1998 Aug;92(8):993-9. doi: 10.1016/s0954-6111(98)90343-2.
In chronic obstructive pulmonary disease (COPD) which consists of emphysema and chronic bronchitis, alveolar tissue and/or bronchiolar walls are progressively destroyed. This suggests cell death by necrosis and/or apoptosis although no direct evidence of apoptosis has been reported. It was speculated that the apoptosis-related factors are associated with the progression of COPD. Fas/Apo-1 receptor (Fas), Fas ligand (Fas-L) and soluble Fas ligand (sFas-L) are inducers, while soluble Fas (sFas) is an inhibitor of apoptosis. In this study, plasma sFas and sFas-L were measured in 19 COPD patients receiving supplemental O2 (severe COPD) and 20 COPD patients not receiving supplemental O2 (mild/moderate COPD). Twenty-two age- and sex-matched healthy volunteers (healthy controls) and 20 patients receiving supplemental O2 and with level of hypoxaemia similar to severe COPD due to other pulmonary diseases (disease controls) were also examined. Plasma sFas-L was within normal limits in all groups. Plasma sFas levels were similar among healthy controls, disease controls, and mild/moderate COPD patients, but significantly increased in severe COPD (2.6 +/- 1.1, 2.6 +/- 0.2, 2.8 +/- 0.2 and 4.8 +/- 1.0 ng ml-1, respectively). Although PaO2 was lower in severe COPD than in mild/moderate COPD, and PaCO2 was higher in severe COPD than in mild/moderate COPD, they were close between severe COPD and disease controls. Tumour necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and C-reactive protein (CRP) were increased in patients with COPD, but were similar in both severe and mild/moderate COPD patients. We conclude that increased plasma sFas, which is independent of hypoxaemia, and increases in PaCO2, TNF-alpha, IL-6 and inflammation, may be associated with progression of COPD.
在由肺气肿和慢性支气管炎组成的慢性阻塞性肺疾病（COPD）中，肺泡组织和/或细支气管壁会逐渐遭到破坏。这表明存在坏死和/或凋亡导致的细胞死亡，尽管尚未有凋亡的直接证据报道。据推测，凋亡相关因子与COPD的进展有关。Fas/Apo-1受体（Fas）、Fas配体（Fas-L）和可溶性Fas配体（sFas-L）是凋亡诱导剂，而可溶性Fas（sFas）是凋亡抑制剂。在本研究中，对19名接受补充氧气治疗的COPD患者（重度COPD）和20名未接受补充氧气治疗的COPD患者（轻度/中度COPD）测定了血浆sFas和sFas-L。还检查了22名年龄和性别匹配的健康志愿者（健康对照组）以及20名因其他肺部疾病接受补充氧气且低氧血症水平与重度COPD相似的患者（疾病对照组）。所有组的血浆sFas-L均在正常范围内。健康对照组、疾病对照组和轻度/中度COPD患者的血浆sFas水平相似，但在重度COPD患者中显著升高（分别为4.8±1.0、2.8±0.2、2.6±0.2和2.6±1.1 ng/ml）。尽管重度COPD患者的PaO2低于轻度/中度COPD患者，且重度COPD患者的PaCO2高于轻度/中度COPD患者，但重度COPD患者与疾病对照组之间的数值相近。COPD患者的肿瘤坏死因子-α（TNF-α）、白细胞介素6（IL-6）和C反应蛋白（CRP）升高，但重度和轻度/中度COPD患者的这些指标相似。我们得出结论，血浆sFas升高独立于低氧血症，且PaCO2、TNF-α、IL-6升高及炎症反应可能与COPD的进展有关。
