Paeng N, Morikawa A, Kato Y, Sugiyama T, Koide N, Yoshida T, Yokochi T
Department of Microbiology and Immunology, and Research Center for Infectious Disease, Aichi Medical University, Japan.
Microbiol Immunol. 1999;43(1):45-52. doi: 10.1111/j.1348-0421.1999.tb02371.x.
An experimental model for autoimmune enterocolitis was produced in mice by repeated immunization of homologous colon extract together with Klebsiella 03 lipopolysaccharide (KO3 LPS) as an immunological adjuvant. Histological changes in the intestinal lesions were characterized by infiltration with polymorphonuclear leukocytes in the lamina propria, muscularis mucosae and submucosa of repeatedly immunized mice. No such intestinal lesions were produced in mice receiving injections of colon extract alone or KO3 LPS alone. Development of the autoantibody and delayed-type hypersensitivity against colon extract were found in mice immunized with the mixture of colon extract and KO3 LPS. Distinct positive staining was detected specifically on the columnar epithelium of villi. Sera from hyperimmunized mice defined organ-specific antigens present in the intestine. Therefore, it was suggested that the intestinal lesions might be caused by an autoimmune mechanism.
通过将同源结肠提取物与作为免疫佐剂的肺炎克雷伯菌03脂多糖（KO3 LPS）反复免疫小鼠，建立了自身免疫性小肠结肠炎的实验模型。反复免疫小鼠的肠道病变的组织学变化特征是固有层、黏膜肌层和黏膜下层有多形核白细胞浸润。单独注射结肠提取物或单独注射KO3 LPS的小鼠未出现此类肠道病变。在用结肠提取物和KO3 LPS混合物免疫的小鼠中发现了针对结肠提取物的自身抗体和迟发型超敏反应。在绒毛的柱状上皮上特异性检测到明显的阳性染色。高免疫小鼠的血清确定了肠道中存在的器官特异性抗原。因此，提示肠道病变可能由自身免疫机制引起。
