Zielonka T M, Demkow U, Filewska M, Bialas-Chromiec B, Zycinska K, Radzikowska E, Korzeniewska M, Wardyn K A, Kus J, Skopinska-Rozewska E
Department of Family Medicine, Warsaw Medical University, Poland.
J Physiol Pharmacol. 2008 Dec;59 Suppl 6:781-9.
Angiogenesis has been implicated in the pathogenesis of interstitial lung diseases. A correlation between serum angiogenic cytokines level of patients with idiopathic pulmonary fibrosis and radiographic manifestations or functional pulmonary changes has been described, but the role of angiogenesis in the pathogenesis of other interstitial lung diseases such as silicosis and pulmonary Langerhans cell histiocytosis remains unclear. The aim of the study was to examine the effect of sera from silicosis and pulmonary Langerhans cell histiocytosis patients on angiogenesis induced by human mononuclear cells (MNC) in relation to pulmonary function. The study population consisted of 12 patients with silicosis, 12 patients with pulmonary Langerhans cell histiocytosis (PLH), and 14 healthy volunteers. Spirometry, whole-body plethysmography, static lung compliance (Cst), and diffusing capacity of the lung for CO (DL(CO)) were performed in all patients. As an angiogenic test, leukocyte induced angiogenesis assay according to Sidky and Auerbach was used. Sera from PLH patients exerted a significant inhibitory effect on angiogenesis (P<0.001). Sera from silicosis patients significantly (P<0.001) stimulated angiogenesis compared with sera from healthy donors. However, sera from healthy donors significantly stimulated the angiogenic activity of MNC compared with the control with PBS. The mean value of DL(CO) was significantly lower in the group of patients with PLH compared with patients with silicosis (P<0.05). A significant correlation between angiogenesis index and DL(CO) was observed (P<0.05). No significant correlation between the angiogenesis index and other functional parameters was found. Sera from interstitial lung diseases patients and healthy donors constitute a source of mediators modulating angiogenesis. Sera from silicosis patients stimulate neovascularization but sera from PLH patients exert an inhibitory effect on angiogenesis. A correlation between serum angiogenic activity and DL(CO) was found.
血管生成与间质性肺疾病的发病机制有关。已有研究描述了特发性肺纤维化患者血清血管生成细胞因子水平与影像学表现或肺功能变化之间的相关性，但血管生成在矽肺和肺朗格汉斯细胞组织细胞增多症等其他间质性肺疾病发病机制中的作用仍不清楚。本研究的目的是探讨矽肺和肺朗格汉斯细胞组织细胞增多症患者血清对人单核细胞（MNC）诱导的血管生成的影响及其与肺功能的关系。研究对象包括12例矽肺患者、12例肺朗格汉斯细胞组织细胞增多症（PLH）患者和14名健康志愿者。对所有患者进行了肺活量测定、体描法、静态肺顺应性（Cst）和肺一氧化碳弥散量（DL(CO)）检测。作为血管生成试验，采用了根据Sidky和Auerbach方法进行的白细胞诱导血管生成试验。PLH患者的血清对血管生成有显著抑制作用（P<0.001）。与健康供体的血清相比，矽肺患者的血清显著（P<0.001）刺激血管生成。然而，与用PBS作为对照相比，健康供体的血清显著刺激MNC的血管生成活性。PLH患者组的DL(CO)平均值显著低于矽肺患者组（P<0.05）。观察到血管生成指数与DL(CO)之间存在显著相关性（P<0.05）。未发现血管生成指数与其他功能参数之间存在显著相关性。间质性肺疾病患者和健康供体的血清构成了调节血管生成的介质来源。矽肺患者的血清刺激新血管形成，但PLH患者的血清对血管生成有抑制作用。发现血清血管生成活性与DL(CO)之间存在相关性。
