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Production of plasminogen activator by alveolar macrophages in normal subjects and patients with interstitial lung disease.正常受试者和间质性肺疾病患者肺泡巨噬细胞纤溶酶原激活物的产生。
Thorax. 1988 Jul;43(7):508-15. doi: 10.1136/thx.43.7.508.
2
Abnormalities in pathways of alveolar fibrin turnover among patients with interstitial lung disease.间质性肺疾病患者肺泡纤维蛋白周转途径的异常。
Am Rev Respir Dis. 1986 Mar;133(3):437-43. doi: 10.1164/arrd.1986.133.3.437.
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Degradation of fibrin and elastin by intact human alveolar macrophages in vitro. Characterization of a plasminogen activator and its role in matrix degradation.人肺泡巨噬细胞在体外对纤维蛋白和弹性蛋白的降解。纤溶酶原激活物的特性及其在基质降解中的作用。
J Clin Invest. 1984 Mar;73(3):806-15. doi: 10.1172/JCI111275.
4
Association between alveolar macrophage plasminogen activator activity and indices of lung function in young cigarette smokers.年轻吸烟者肺泡巨噬细胞纤溶酶原激活物活性与肺功能指标之间的关联。
Am Rev Respir Dis. 1988 Dec;138(6):1422-8. doi: 10.1164/ajrccm/138.6.1422.
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Phenotypic analysis of alveolar macrophages in normal subjects and in patients with interstitial lung disease.正常受试者和间质性肺疾病患者肺泡巨噬细胞的表型分析。
Thorax. 1986 Jun;41(6):429-34. doi: 10.1136/thx.41.6.429.
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Increased alveolar plasminogen activator in early asbestosis.早期石棉沉着病中肺泡纤溶酶原激活剂增加。
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Production of plasminogen activator and plasminogen activator inhibitors by alveolar macrophages in control subjects and AIDS patients.健康对照者和艾滋病患者的肺泡巨噬细胞产生纤溶酶原激活物及纤溶酶原激活物抑制剂的情况。
AIDS. 1996 Mar;10(3):283-90. doi: 10.1097/00002030-199603000-00007.
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Smoking and interstitial lung disease. The effect of cigarette smoking on the incidence of pulmonary histiocytosis X and sarcoidosis.吸烟与间质性肺疾病。吸烟对肺组织细胞增多症X和结节病发病率的影响。
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Bronchoalveolar macrophages in sarcoidosis and cryptogenic fibrosing alveolitis.结节病和隐源性纤维性肺泡炎中的支气管肺泡巨噬细胞。
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10
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Secretion of plasminogen activator inhibitor by normal rat pleural leukocytes in culture.培养的正常大鼠胸膜白细胞纤溶酶原激活物抑制剂的分泌
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2
Induction of macrophage plasminogen activator by asbestos is independent of PKC activation.石棉诱导巨噬细胞纤溶酶原激活剂与蛋白激酶C激活无关。
Arch Toxicol. 1991;65(5):386-9. doi: 10.1007/BF02284261.

本文引用的文献

1
Cell surface alterations associated with exposure of leukemia L1210 cells to fluorouracil.白血病L1210细胞暴露于氟尿嘧啶后相关的细胞表面改变。
Cancer Res. 1980 Feb;40(2):322-4.
2
Activation of the classical pathway of complement by Hageman factor fragment.凝血因子片段激活补体经典途径。
J Exp Med. 1981 Mar 1;153(3):665-76. doi: 10.1084/jem.153.3.665.
3
Chronic inflammatory bowel disease--increased plasminogen activator secretion by mononuclear phagocytes.慢性炎症性肠病——单核吞噬细胞纤溶酶原激活物分泌增加。
Clin Exp Immunol. 1982 Apr;48(1):256-60.
4
The development of granulomatous pulmonary inflammation in rabbits by aerosol challenge. I. Release of plasminogen activator by alveolar macrophages.通过气溶胶激发在兔中诱导肉芽肿性肺炎。I. 肺泡巨噬细胞释放纤溶酶原激活物
Cell Immunol. 1982 Feb;67(1):90-100. doi: 10.1016/0008-8749(82)90201-5.
5
The production of plasminogen activator by afferent but not efferent lymph cells emigrating from chronic granulomatous lesions in sheep.从绵羊慢性肉芽肿病变中移出的传入而非传出淋巴细胞产生纤溶酶原激活物。
J Immunol. 1982 Mar;128(3):1076-82.
6
Content and characterization of plasminogen activators in human lung tumors and normal lung tissue.人肺肿瘤和正常肺组织中纤溶酶原激活剂的含量及特性
Cancer Res. 1980 Mar;40(3):841-8.
7
The cellular target for the plasminogen activator, urokinase, in human fibroblasts - 66 000 dalton protein.纤溶酶原激活剂尿激酶在人成纤维细胞中的细胞靶点——66000道尔顿蛋白质。
Biochim Biophys Acta. 1982 Apr 29;720(2):141-6. doi: 10.1016/0167-4889(82)90005-2.
8
Human alveolar macrophage-derived chemotactic factor for neutrophils. Stimuli and partial characterization.人肺泡巨噬细胞来源的嗜中性粒细胞趋化因子。刺激因素及部分特性
J Clin Invest. 1980 Sep;66(3):473-83. doi: 10.1172/JCI109878.
9
Cultured bovine endothelial cells produce both urokinase and tissue-type plasminogen activators.培养的牛内皮细胞可产生尿激酶和组织型纤溶酶原激活剂。
J Cell Biol. 1982 Sep;94(3):631-6. doi: 10.1083/jcb.94.3.631.
10
Cigarette smoking and lung destruction. Accumulation of neutrophils in the lungs of cigarette smokers.吸烟与肺组织破坏。吸烟者肺部中性粒细胞的聚集。
Am Rev Respir Dis. 1983 Nov;128(5):833-8. doi: 10.1164/arrd.1983.128.5.833.

正常受试者和间质性肺疾病患者肺泡巨噬细胞纤溶酶原激活物的产生。

Production of plasminogen activator by alveolar macrophages in normal subjects and patients with interstitial lung disease.

作者信息

Robinson B W

机构信息

University Department of Medicine, Queen Elizabeth II Medical Centre, Nedlands, Western Australia.

出版信息

Thorax. 1988 Jul;43(7):508-15. doi: 10.1136/thx.43.7.508.

DOI:10.1136/thx.43.7.508
PMID:3212749
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC461353/
Abstract

Increased production of the serum protease plasminogen activator is associated with tissue damage. The in vitro production of plasminogen activator by alveolar macrophages obtained by bronchoalveolar lavage was studied in 22 normal subjects and 28 patients with interstitial lung disease to determine whether plasminogen activator is produced by normal alveolar macrophages and whether this is increased in patients with interstitial lung disease. Plasminogen activator activity, measured with an iodine-125 labelled fibrin release assay, was found to be dependent on time, effector cell numbers, and plasminogen concentration. Plasminogen activator production by alveolar macrophages from 14 normal non-smokers and eight normal smokers was similar and the mean value was 0.78 (SEM 0.16) urokinase (UK) units x 10(-8)/cell/hour. Alveolar macrophages from the seven patients with cryptogenic fibrosing alveolitis and six patients with histiocytosis-X produced more plasminogen activator (1.89 (0.25) and 4.54 (1.3) x 10(-8) UK units/cell/hour respectively) than macrophages from normal subjects (p less than 0.05), whereas those from 15 patients with sarcoidosis did not (1.09 (0.2) x 10(-8) UK units/cell/hour). Exposure of normal alveolar macrophages to immune complexes enhanced plasminogen activator production to 2.07 (0.27) x 10(-8) UK units/cell/hour, whereas exposure to products of activated T cells and to purified gamma interferon reduced plasminogen activator production (to 0.38 (0.11) and 0.62 (0.11) x 10(-8) UK units/cell/hour respectively). These studies show that plasminogen activator is produced by normal human alveolar macrophages and that its production is increased in patients with cryptogenic fibrosing alveolitis and histiocytosis-X.

摘要

血清蛋白酶纤溶酶原激活物产量增加与组织损伤有关。通过支气管肺泡灌洗获取肺泡巨噬细胞,研究了22名正常受试者和28名间质性肺疾病患者肺泡巨噬细胞在体外产生纤溶酶原激活物的情况,以确定正常肺泡巨噬细胞是否产生纤溶酶原激活物,以及间质性肺疾病患者其产量是否增加。用碘 - 125标记的纤维蛋白释放试验测定纤溶酶原激活物活性,发现其依赖于时间、效应细胞数量和纤溶酶原浓度。14名正常不吸烟者和8名正常吸烟者的肺泡巨噬细胞产生纤溶酶原激活物的情况相似,平均值为0.78(标准误0.16)尿激酶(UK)单位×10⁻⁸/细胞/小时。7名隐源性纤维性肺泡炎患者和6名组织细胞增多症X患者的肺泡巨噬细胞产生的纤溶酶原激活物(分别为1.89(0.25)和4.54(1.3)×10⁻⁸ UK单位/细胞/小时)比正常受试者的巨噬细胞更多(p<0.05),而15名结节病患者的肺泡巨噬细胞则不然(1.09(0.2)×10⁻⁸ UK单位/细胞/小时)。正常肺泡巨噬细胞暴露于免疫复合物时,纤溶酶原激活物产量增加至2.07(0.27)×10⁻⁸ UK单位/细胞/小时,而暴露于活化T细胞产物和纯化的γ干扰素时,纤溶酶原激活物产量降低(分别降至0.38(0.11)和0.62(0.11)×10⁻⁸ UK单位/细胞/小时)。这些研究表明,正常人肺泡巨噬细胞可产生纤溶酶原激活物,且隐源性纤维性肺泡炎和组织细胞增多症X患者其产量增加。