Zielonka T M, Demkow U, Zycinska K, Filewska M, Korzeniewska M, Radzikowska E, Bialas-Chromiec B, Kus J, Wardyn K A, Skopinska-Rozewska E
Department of Family Medicine, Warsaw Medical University, Warsaw, Poland.
J Physiol Pharmacol. 2008 Dec;59 Suppl 6:791-800.
Systemic autoimmune diseases, such as vasculitis and collagen diseases, are characterized by chronic inflammation. Mutual interrelationship between angiogenesis and chronic inflammation has already been demonstrated. The aim of the study was to examine the effect of sera from patients with systemic autoimmune diseases on angiogenesis induced by human mononuclear cells. The study population consisted of 43 patients with a systemic autoimmune disease associated with pulmonary manifestations, divided into three groups: 14 with Wegener's granulomatosis (WG), 13 with systemic sclerosis (SS), and 16 with collagen vascular diseases (CVD) such as rheumatoid arthritis, systemic lupus erythematosus, and dermatomyositis. The control group consisted of 15 healthy volunteers. Clinical status was evaluated using a questionnaire. Standard chest radiographs were performed in all patients. Pulmonary function tests were performed according to the ERS standards. An animal model of a leukocyte-induced angiogenesis assay was used as an angiogenic test. Sera from WG and CVD patients significantly stimulated angiogenesis compared with healthy subjects (P<0.001). On the other hand, sera from healthy donors exerted a proangiogenic effect compared with PBS. In contrast, sera from SS patients significantly (P<0.001) inhibited angiogenesis compared with sera from healthy subjects and PBS. Proangiogenic effect of sera from systemic diseases patients depended on radiological changes. No significant correlation between a degree of dyspnea or functional pulmonary tests and the number of new vessels or angiogenesis index was found. Sera from patients with systemic autoimmune diseases and healthy people constitute the source of mediators modulating angiogenesis. These modulatory effects differ depending on the disease entity.
系统性自身免疫性疾病,如血管炎和胶原病,其特征为慢性炎症。血管生成与慢性炎症之间的相互关系已得到证实。本研究的目的是检测系统性自身免疫性疾病患者血清对人单核细胞诱导的血管生成的影响。研究对象包括43例伴有肺部表现的系统性自身免疫性疾病患者,分为三组:14例韦格纳肉芽肿(WG)患者、13例系统性硬化症(SS)患者和16例胶原血管病(CVD)患者,如类风湿关节炎、系统性红斑狼疮和皮肌炎。对照组由15名健康志愿者组成。使用问卷评估临床状况。所有患者均进行标准胸部X线检查。根据欧洲呼吸学会标准进行肺功能测试。使用白细胞诱导血管生成试验的动物模型作为血管生成检测方法。与健康受试者相比,WG和CVD患者的血清显著刺激血管生成(P<0.001)。另一方面,与磷酸盐缓冲液(PBS)相比,健康供体的血清具有促血管生成作用。相比之下,与健康受试者和PBS的血清相比,SS患者的血清显著(P<0.001)抑制血管生成。系统性疾病患者血清的促血管生成作用取决于放射学改变。未发现呼吸困难程度或肺功能测试与新血管数量或血管生成指数之间存在显著相关性。系统性自身免疫性疾病患者和健康人的血清构成了调节血管生成的介质来源。这些调节作用因疾病类型而异。