Bryson D G, McConnell S, McAliskey M, McNulty M S
Veterinary Research Laboratories, Stormont, Belfast, Northern Ireland, United Kingdom.
Vet Pathol. 1991 Jul;28(4):286-92. doi: 10.1177/030098589102800404.
Ultrastructural changes occurred in alveolar epithelium in the acute and repair stages of induced respiratory syncytial virus pneumonia induced in eight calves (calf Nos. 1-7, 3 to 6 days old and calf No. 8, 2 weeks old), using a bovine strain of respiratory syncytial virus. Five of the calves were Friesians, three were Hereford x Friesians, and all were male. Tissues from three mock-infected control calves (two Friesian, one Hereford x Friesian) were also examined. Evidence of respiratory syncytial virus infection was observed in both type I and type II pneumocytes from day 4 to day 8 after infection. Infection of type I pneumocytes frequently resulted in necrosis. The response of type II pneumocytes to respiratory syncytial virus infection varied and included hypertrophy, hyperplasia, and syncytial formation. In some infected type II pneumocytes, there were numerous irregular projections of the cell surface, associated with viral budding. Hypertrophy and hyperplasia of type II pneumocytes, epithelial syncytium formation, and irregular cytoplasmic projections from epithelial cells caused considerable thickening of respiratory membrane and occlusion of alveolar lumina. Neutrophils were frequently observed in close association with virus-infected epithelial cells, but evidence of respiratory syncytial virus infection and replication was not observed in alveolar macrophages or neutrophils. Proliferation of type II pneumocytes appeared to play a major role in maintaining the integrity of the alveolar epithelium during the acute stage of the experimental pneumonia. Increased numbers of type II pneumocytes were present on alveolar walls, particularly from 4 to 8 days after infection, and some alveoli were lined entirely by this cell type. In some areas, however, squamous epithelial cells were also involved in covering exposed alveolar basement membrane.
用牛呼吸道合胞病毒株感染8头犊牛(1至7号犊牛,3至6日龄;8号犊牛,2周龄)诱发呼吸道合胞病毒肺炎,观察其急性和修复阶段肺泡上皮的超微结构变化。5头犊牛为弗里斯兰牛,3头为赫里福德×弗里斯兰杂交牛,均为雄性。还检查了3头模拟感染对照犊牛(2头弗里斯兰牛,1头赫里福德×弗里斯兰杂交牛)的组织。感染后第4天至第8天,在Ⅰ型和Ⅱ型肺细胞中均观察到呼吸道合胞病毒感染的证据。Ⅰ型肺细胞感染常导致坏死。Ⅱ型肺细胞对呼吸道合胞病毒感染的反应各异,包括肥大、增生和多核巨细胞形成。在一些受感染的Ⅱ型肺细胞中,细胞表面有许多不规则突起,与病毒出芽有关。Ⅱ型肺细胞的肥大、增生、上皮多核巨细胞形成以及上皮细胞不规则的胞质突起导致呼吸膜明显增厚和肺泡腔闭塞。经常观察到中性粒细胞与病毒感染的上皮细胞紧密相连,但在肺泡巨噬细胞或中性粒细胞中未观察到呼吸道合胞病毒感染和复制的证据。在实验性肺炎急性期,Ⅱ型肺细胞的增殖似乎在维持肺泡上皮的完整性方面起主要作用。肺泡壁上Ⅱ型肺细胞数量增加,尤其是在感染后4至8天,一些肺泡完全由这种细胞类型覆盖。然而,在一些区域,鳞状上皮细胞也参与覆盖暴露的肺泡基底膜。