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目的 观察严重急性呼吸综合征(SARS)肺纤维化的表现,初步探讨SARS时肺纤维化的发病机制。方法 采用光镜、纤维化组织化学染色、免疫组织化学SP法以鼠抗Ⅲ型胶原、鼠抗α- 平滑肌肌动蛋白(α- SMA)、兔抗Fas、兔抗Fas 配体(FasL)、兔抗转化生长因子β1- (TGF β1)对4 例SARS死亡病例的肺组织纤维化改变进行重点观察。结果 4 例肺组织中存在不同程度的纤维化改变。表现为肺泡腔内纤维素性渗出物积聚及机化,甚而形成“团块状纤维样”结构;肺泡间隔增厚,成纤维细胞增生,可见胶原纤维条索;组织化学染色及Ⅲ型胶原染色证实以Ⅲ型和Ⅰ型胶原纤维增生为主;肺泡腔内的纤维化与肺泡外间质融合形成肺的实变。免疫组织化学检测成纤维细胞表达αSMA、脱落的肺泡上皮细胞表达Fas、FasL、肺泡上皮细胞和单核细胞的细胞浆内表达TGF- β1。结论 SARS患者的肺组织早期即有纤维化的征象,其纤维化的发生是各种效应细胞、炎症介质及细胞因子共同参与的结果。
Objective To observe the manifestation of pulmonary fibrosis in severe acute respiratory syndrome (SARS) and to explore the pathogenesis of pulmonary fibrosis in SARS. Methods Anti-type Ⅲ collagen, α-SMA, rabbit anti-Fas, rabbit anti-Fas ligand (FasL) were detected by light microscopy and histochemical staining. Rabbit anti-transforming growth factor β1- (TGF β1) focus on the changes of lung fibrosis in 4 SARS death cases. Results In 4 cases, there were different degrees of fibrosis in the lung tissue. Manifested as alveolar cavity of cellulose exudate accumulation and mechanization, and even the formation of “lumpy fibrous” structure; alveolar septum thickening, fibroblast proliferation, visible collagen fibers; histochemical staining and collagen type Ⅲ Confirmed to type Ⅲ and type Ⅰ collagen fibers mainly hyperplasia; alveolar intraluminal fibrosis and alveolar extraluminal fusion to form the consolidation of the lung. The expression of α SMA in fibroblasts was detected by immunohistochemistry, and the expressions of Fas, FasL, alveolar epithelial cells and monocytes in exfoliated alveolar epithelial cells were positive for TGF-β1. Conclusion The lungs of patients with SARS are characterized by early fibrosis. The occurrence of fibrosis is the result of the joint participation of various effector cells, inflammatory mediators and cytokines.