van Marck E A, Stocker S, Grimaud J A, Kestens L, Gigase P L, Deelder A M
Experientia. 1980 Sep 15;36(9):1116-8. doi: 10.1007/BF01966002.
An experimental model of schistosomal portal fibrosis is described. Sepharose beads the size of schistosome eggs, loaded or not with soluble egg antigen (SEA) from Schistosoma mansoni, are injected into the coecal vein of C3H/Sn mice and become embolized in the liver. Only SEA-coated beads evoke a granulomatous reaction; this is enhanced by simultaneous priming of the mice with spleen cells from Schistosoma mansoni-infected syngeneic animals. The fibrosis, which ensues around the beads, is stable and is much more evident after priming. Preliminary collagen tissue immunotyping reveals the presence of collagen deposits of types I and III collagen. Type IV collagen remains unchanged in the portal tracts. The model appears to be well suited for studies of the pathogenesis of portal fibrosis.
本文描述了一种血吸虫性门脉纤维化的实验模型。将大小与血吸虫卵相同、负载或未负载曼氏血吸虫可溶性虫卵抗原(SEA)的琼脂糖珠注入C3H/Sn小鼠的盲肠静脉,使其在肝脏中形成栓塞。只有包被SEA的珠子会引发肉芽肿反应;用来自曼氏血吸虫感染的同基因动物的脾细胞对小鼠进行同步致敏可增强这种反应。在珠子周围随后发生的纤维化是稳定的,致敏后更为明显。初步的胶原组织免疫分型显示存在I型和III型胶原沉积。IV型胶原在门脉区保持不变。该模型似乎非常适合用于研究门脉纤维化的发病机制。