Kogan E A, Kichigina O N, Demura S A, Osipenko V I
Arkh Patol. 2012 May-Jun;74(3):37-43.
Sarcoidosis is a group of diseases with chronic immune inflammation and granulomas formation in the lung, lymph nodes, and others organs. Under progress of disease remodeling of the lung tissue occurs and at 20-25% of patient with sarcoidosis lung fibrosis is developed. We studied biopsies from 50 patients with sarcoidosis and 10 biopsies of pathological intact lung tissue as a control group. Roentgenologic, morphologic and immunohistochemical methods with using of mono- and polyclonal antibody to MMP 1, 2, 9 and TIMP-1, PCNA, aSMA, apo-CAS were realized. The expression levels of growth factors, apoptosis, MMPs, TIMPs were different in various clinic-morphological courses of sarcoidosis. As a rule under sarcoidosis deep remodeling of lung tissue didn't occur in spite of granulomatous inflammation. Granulomatous process, alveolitis (bronchiolitis) and sclerotic changes resulted in alteration of the lung. Cells of sarcoidosis granulomas, produced low level of MMPs and TIMP can't induce evident fibrosis and so hypertension is absent or becomes apparent in the slight form. It apparently can be link with localization of pathologic process in lung tissue without any alterations in the bronchoalveolar zone. Alveolitis under sarcoidosis conditions is notable for low activity of inflammation and doesn't result in interstitial fibrosis developing.
结节病是一组在肺部、淋巴结及其他器官发生慢性免疫炎症和肉芽肿形成的疾病。在疾病进展过程中，肺组织会发生重塑，20%至25%的结节病患者会发展为肺纤维化。我们研究了50例结节病患者的活检样本，并选取10例病理正常的肺组织活检样本作为对照组。采用了X线、形态学和免疫组化方法，使用了针对基质金属蛋白酶1、2、9和金属蛋白酶组织抑制因子-1、增殖细胞核抗原、α平滑肌肌动蛋白、载脂蛋白-CAS的单克隆和多克隆抗体。在结节病的不同临床形态学病程中，生长因子、细胞凋亡、基质金属蛋白酶、金属蛋白酶组织抑制因子的表达水平有所不同。通常情况下，尽管存在肉芽肿性炎症，但结节病时肺组织的深度重塑并未发生。肉芽肿形成过程、肺泡炎（细支气管炎）和硬化性改变导致了肺部的改变。结节病肉芽肿细胞产生的基质金属蛋白酶和金属蛋白酶组织抑制因子水平较低，无法诱导明显的纤维化，因此高血压不存在或仅以轻微形式出现。这显然可能与肺组织中病理过程的定位有关，而支气管肺泡区域没有任何改变。结节病情况下的肺泡炎以炎症活动度低为特征，不会导致间质纤维化的发展。
