Carrasco L, de Lara F C, Gómez-Villamandos J C, Bautista M J, Villeda C J, Wilkinson P J, Sierra M A
Departamento de Anatomía y Anatomía Patológica Comparadas, Facultad de Veterinaria, Universidad de Córdoba, Spain.
Res Vet Sci. 1996 Nov;61(3):193-8. doi: 10.1016/s0034-5288(96)90062-4.
Recent studies of pulmonary intravascular macrophages have led to the re-examination of the mechanisms giving rise to alveolar oedema. A highly virulent isolate of African swine fever virus was replicated in pulmonary intravascular macrophages, interstitial and alveolar macrophages, fibroblasts and neutrophils. The alveolar oedema-characteristic of acute forms of African swine fever-and the vascular changes observed, which consisted of the formation of fibrin microthrombi in septal capillaries and the vacuolisation of endothelial cells, may have been due, however, to the activation of pulmonary intravascular macrophages, and not to the cytopathic effect subsequent to the replication of the African swine fever virus. Furthermore, it was observed that virus replication in cells not belonging to the mononuclear phagocyte system-such as fibroblasts and neutrophils-occurred earlier than in cells belonging to that system.
最近对肺血管内巨噬细胞的研究促使人们重新审视引发肺泡水肿的机制。一种高致病性非洲猪瘟病毒毒株在肺血管内巨噬细胞、间质和肺泡巨噬细胞、成纤维细胞及中性粒细胞中复制。然而，非洲猪瘟急性形式所特有的肺泡水肿以及所观察到的血管变化，包括间隔毛细血管中纤维蛋白微血栓的形成和内皮细胞的空泡化，可能是由于肺血管内巨噬细胞的激活，而非非洲猪瘟病毒复制后的细胞病变效应。此外，还观察到病毒在不属于单核吞噬细胞系统的细胞（如成纤维细胞和中性粒细胞）中的复制比在该系统的细胞中更早发生。
