摘要
目的通过对严重急性呼吸综合征(SARS)肺组织中CD34、血管内皮生长因子(VEGF)和细胞间黏附分子(ICAM-1)表达水平的检测对其发病机制进行探讨。方法将7例死亡SARS病例及同期6例具有急性肺损伤性临床表现的非SARS死亡病例肺标本对照进行HE染色及CD34、VEGF、ICAM-1免疫组化检查,并对免疫组化染色结果进行图像分析。结果CD34染色结果显示SARS组肺毛细血管内皮细胞着色浓重胞膜完整、排列紊乱但细胞连续性好,平均光密度值(MOD)为0.2843±0.1033;非SARS组肺组织CD34染色浅淡、不连续,MOD值为0.1297±0.0073,两组结果差异有显著性(P=0.0074);不合并细菌或真菌感染SARS标本的MOD值为0.3428±0.0316,与非SARS组结果差异有显著性(P<0.0001)。SARS组VEGF阳性染色MOD为0.1253±0.042,与非SARS组0.1143±0.0252相比,结果差异无统计学意义(P=0.5888)。两组ICAM-1阳性染色MOD值差异无统计学意义;但不合并感染的SARS标本ICAM-1MOD值为0.2557±0.0452,与非SARS组0.182±0.017相比,结果差异有统计学意义(P=0.006)。结论SARS肺脏中内皮细胞的损伤程度较之其他原因引起的肺组织损伤轻,ICAM-1和VEGF表达也存在不同,这些差异可能反映了SARS肺损伤的特殊性,对解释SARS的临床和病理生理过程具有一定意义。
Purpose To study the possible pathogenesis of severe acute respiratory syndrome （SARS） by comparing the protein expression of CD34, VEGF and ICAM-1 in SARS lungs with those in non-SARS lung injury. Methods Specimens, from 7 cases of diagnosed SARS and 6 non-SARS cases died with acute lung injury, were examined by routine HE and immunohistochemical stains of CD34, VEGF and ICAM-1, and then image analysis. Results The blood vessels in SARS lungs outlined the alveolus clearly, and its mean optical density （MOD） was 0. 284 3 ± 0. 103 3, which was significantly greater than that of non-SARS lungs （0. 129 7± 0. 007 3 ,P =0. 007 4）. The MOD of VEGF of the two groups had no statistical difference. The MOD of ICAM-1 in SARS lung was significandy increased in the cases without infectious morbidity （P = 0. 041 6）. Conclusion The endothelial cells in SARS lungs are injured not so seriously as compared with those of infectious lung injury. The expression of ICAM-1 and VEGF is also different, which may reflect the characteristics of SARS lung injury and explain the clinical process of SARS partly.
出处
《临床与实验病理学杂志》
CAS
CSCD
北大核心
2007年第2期182-185,共4页
Chinese Journal of Clinical and Experimental Pathology
基金
国家自然科学基金(30340030)
