Fukuda Y, Ferrans V J
Pathology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892.
J Submicrosc Cytol Pathol. 1988 Jan;20(1):15-23.
To study the morphologic alterations of pulmonary elastic fibers in cynomolgus monkeys with paraquat toxicity, peroxidase- and ferritin-labeled antielastin antibodies were used for the light and electron microscopic localization of elastin. One week after paraquat, alveolitis, tissue damage and alveolar dilatation were present; elastic fibers were frayed and more diffusely and intensely stained than those of control animals. In the latter, staining was localized in peripheral regions of the amorphous components and, to a lesser extent, in some microfibrils of elastic fibers. At 3 to 4 weeks, diffuse staining was evident in damaged interstitial elastic fibers and in newly formed elastic fibers in areas of intraalveolar fibrosis. At 8 weeks, the interstitium contained many elastic fibers which showed staining only in peripheral regions of the amorphous components. These observations suggest that: 1) preembedding immunohistochemical staining for elastin is localized in peripheral regions of normal elastic fibers because the antielastin antibody can penetrate into mature and undamaged amorphous components only to a very limited extent; 2) in early stages of paraquat toxicity this staining is more diffuse and intense because elastase from inflammatory cells partially degrades the elastic fibers and permits greater penetration of the antibody into the amorphous materials; 3) in later stages the staining pattern returns to normal as inflammation subsides and elastic fibers are repaired; however, newly formed elastic fibers in areas of intraalveolar fibrosis stain diffusely, reflecting increased penetration of the antibody because of immaturity and incomplete cross-linking, and 4) degeneration of elastic fibers of alveolar walls in paraquat lung may lead to alveolar dilatation, which is associated with irregular fibrosis and constitutes one of the processes of pulmonary structural remodeling in paraquat lung.(ABSTRACT TRUNCATED AT 250 WORDS)
为研究百草枯中毒食蟹猴肺弹性纤维的形态学改变,采用过氧化物酶和铁蛋白标记的抗弹性蛋白抗体对弹性蛋白进行光镜和电镜定位。百草枯中毒1周后,出现肺泡炎、组织损伤和肺泡扩张;弹性纤维磨损,与对照动物相比,染色更弥散、更深。在对照动物中,染色定位于无定形成分的周边区域,在较小程度上也定位于弹性纤维的一些微原纤维中。3至4周时,受损的间质弹性纤维和肺泡内纤维化区域新形成的弹性纤维出现明显的弥散染色。8周时,间质中有许多弹性纤维,仅在无定形成分的周边区域显示染色。这些观察结果表明:1)弹性蛋白的包埋前免疫组化染色定位于正常弹性纤维的周边区域,因为抗弹性蛋白抗体只能非常有限地穿透成熟且未受损的无定形成分;2)在百草枯中毒早期,这种染色更弥散、更深,因为炎症细胞产生的弹性蛋白酶部分降解弹性纤维,使抗体能更大程度地穿透进入无定形物质;3)在后期,随着炎症消退和弹性纤维修复,染色模式恢复正常;然而,肺泡内纤维化区域新形成的弹性纤维呈弥散染色,反映出由于不成熟和不完全交联,抗体的穿透增加;4)百草枯肺中肺泡壁弹性纤维的退变可能导致肺泡扩张,这与不规则纤维化相关,是百草枯肺肺结构重塑的过程之一。(摘要截取自250词)