空肠弯曲杆菌诱发大鼠IgA肾病——肠道感染诱发IgA肾病的作用探讨

IgA nephropathy induced by formalized campylobacter jejunum in rats

为了进一步证实肠道感染在IgA肾病发病中的作用,我们首次应用肠道常见致病菌——空肠弯曲杆菌甲醛化后灌服大鼠,制作IgA肾病模型。结果发现空肠弯曲杆菌组大鼠空肠粘模内含IgA浆细胞增多,26只大鼠中19只肾小球有IgA沉积,其中IgM的合并沉积率为73％,肾组织学改变主要为弥漫系膜基质增生。本实验再次证实了肠道粘膜免疫异常在IgA肾病发病中的作用,以及与IgA肾病肾组织内IgM沉积之间的联系,为今后IgA肾病的研究工作提供了一种新的、可能很有前途的实验模型。

The study for demonstrating the important role of the intestinal mucosa immune system in the pathogenesis of mesangial IgA nephropathy was done by successfully developed IgA nephropathy model in SD rats by giving C-J(4×10~9CFU/2ml)weekly for 3 weeks, Animals were sacrificed at 7, 12, 17, 21 weeks after C-J inoculation. Light microscopy, immunofluorescence and immunoperoxidase stains for kidney, liver and jejunum tissue specimens were performed. IgA deposition in the glomerular mesangial areas and capillary walls, with co-deposition of IgM (73%) IgG (31%) and C3 (63%) were shown in 19 out of 26 rats. The number of IgA-containing plasma cells within mucosa of jejunum of the experimental group were significantly higher than those of the control. The results suggested that abnormal intestinal mucosa immunity induced by oral immunization of formalized C-J was considered to be Important in the pathogenesis of IgA nephropathy.