Hodgson H J, Potter B J, Skinner J, Jewell D P
Gut. 1978 Mar;19(3):225-32. doi: 10.1136/gut.19.3.225.
An experimental colitis in rabbits is described, following the intravenous injection of preformed immune complexes of human serum albumin (HSA) and anti-HSA into non-sensitised rabbits. Tissue damage was localised to the colon by the Auer technique of inducing local non-specific inflammation, by the rectal instillation of dilute formalin. Formalin alone gave transient changes that reverted to normal within 24 hours. In rabbits given intravenous immune complexes formed in antigen-excess, a severe colitis was initiated, with histological features including mucosal ulceration, mixed inflammatory cell infiltration in the lamina propria, and crypt abscess formation. It is possible that immune-complex damage may be one of the pathogenic mechanisms involved in human ulcerative colitis.
本文描述了一种实验性兔结肠炎模型,该模型通过将预先形成的人血清白蛋白(HSA)和抗HSA免疫复合物静脉注射到未致敏的兔子体内构建。通过Auer技术诱导局部非特异性炎症,即经直肠滴注稀释福尔马林,使组织损伤局限于结肠。单独使用福尔马林只会引起短暂变化,24小时内即可恢复正常。给兔子静脉注射抗原过量时形成的免疫复合物后,引发了严重的结肠炎,其组织学特征包括黏膜溃疡、固有层混合性炎症细胞浸润以及隐窝脓肿形成。免疫复合物损伤可能是人类溃疡性结肠炎的致病机制之一。