Pathogenesis of encapsulating peritoneal sclerosis in the role of complement regulatory proteins and glycation

我们从晚期糖基化终产物(AGE)和补体激活的角度探讨了包膜腹膜硬化症(EPS)的机制。腹膜透析患者腹膜间皮细胞和腹膜间质呈AGE、C3、C4和MAC阳性染色。特别是有腹膜炎病史的标本，MAC染色较深。在间皮细胞培养的实验模型中，加入正常人血清(NHS)可观察到H因子、C3和MAC的沉积(P为阴性)，而在NHS前加入P可增强C3和MAC的阳性信号。P可能压倒H，导致间皮细胞表面补体替代途径活化。提示补体替代途径激活可能参与了EPS的发病机制。

We explored the mechanisms of encapsulating peritoneal sclerosis (EPS)in the view point of advanced glycation end product (AGE) and complement activation. Peritoneal mesothelial cell and interstitium of peritoneum derived from the patients of peritoneal dialysis presented positive staining for AGE, C3, C4 and MAC. Especially in the specimens with the cases having peritonitis history, MAC staining were storong. In experimental model of mesothelial cell culture, deposition of factor H, C3 and MAC (properdin (P) was negative) were observed by adding normal human serum (NHS), however, the positive signal of C3 and MAC were enhanced by adding P before NHS. P might overwhelm H and leads complement alternative pathway activation on the surface of mesothelial cell. These results suggested that complement alternative pathway activation might involve the pathogenesis of EPS.