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作 者:张立洁[1] 郎振为[1] 孙琳[1] 孟忻[1] 张世杰[1] 宋晨朝[1] 李俊强[1] 阎惠平[1]
机构地区:[1]首都医科大学附属北京佑安医院病理科,100054
出 处:《中华传染病杂志》2005年第1期46-48,共3页Chinese Journal of Infectious Diseases
基 金:北京市科委科研项目(H030230100130)
摘 要: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 pulmonary fibrosis in severe acute respiratory syndrome (SARS) and to discuss the mechanisms of pulmonary fibrosis in SARS. Methods Hematoxylin and Eosin staining (H&E), histology staining and immuno-histochemical staining (SP methods) were used to investigate the lungs from 4 autopsy cases. Antibodies against collagen type Ⅲ, α-smooth muscle actin(α-SMA), Fas, FasL and transforming growth factor β1(TGF-β1) were used for immunohistochemical studies. Results All these four lung tissues showed different degree of pulmonary fibrosis, including the organization of exudative fibrin, glomerulus-like fibrosis in alveolar spaces, the thickening of the alveolar septum, proliferation of fibroblasts, the hyperplasia of collagen fibers and the consolidation of lungs. Sirius red staining and collagen type Ⅲ staining showed the type Ⅲ and the type Ⅰ collagen fibers were the main components of the hyperplastic collagen fibers. α-SMA were expressed in fibroblasts, immunoreactivity to Fas, FasL, TGF-β1 were all positive and located in plasma of pneumocytes, macrophages and lymphocytes. Conclusions The pulmonary fibrosis can be observed early in SARS patients and the pathogenesis may be involved in the co-effect of many effective cells, inflammatory mediators and cytokines.
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