Heymann nephritis in Lewis rats.

Human membranous nephritis is a major cause of end-stage kidney disease. Active Heymann nephritis (HN) is an auto-immune model of membranous nephritis induced in Lewis rats by immunization with a crude renal tubular antigen (Fx1A) or megalin (gp330). The pathogenesis of HN is through the binding of anti-Fx1A autoantibodies to the auto-antigen expressed on glomerular epithelial cells, resulting in severe glomerular injury and proteinuria. The pathological features of HN include immune deposits in glomeruli and infiltration of glomeruli and the tubulointerstitium by macrophages and T cells. This unit describes the method of the preparation of Fx1A and the induction of HN in Lewis rats by immunization with Fx1A.

[The effect of splenic lymphocytes from oral immune tolerance rats on activity of NF-kappaB p65 in glomerular mesangial cells].

AIM: To explore the effect of splenic lymphocytes from oral immune tolerance rats on NF-kappaB p65 activity in glomerular mesangial cells. METHODS: 10 female Wistar rats with 6-8 weeks of age were divided randomly into two groups, 5 rats for each group. The rats of one group were given through intragastric feeding with 2 mL Fx1A antigen to induce oral immune tolerance, and the rats of the other group only with PBS (as control group). Two weeks later, the rats were sacrificed, and then their spleens were excised and lymphocytes were separated routinely for antigen-specific lymphocytes reaction. The culture supernatants of splenic lymphocytes from oral immune tolerance rats were prepared. The IL-10 level in the supernatants was detected by sandwich ELISA. After the cultured mesangial cells were stimulated with high dose of insulin, the culture supernatants of rat's splenic lymphocytes were added to insulin-treated mesangial cells. Twenty-four hours later, the NF-kappaB p65 activity in mesangial cells was detected by immunohistochemical staining and sandwich ELISA. RESULTS: As compared with control group, the proliferation reaction of splenic lymphocytes from oral immune tolerance rats was inhibited obviously, and IL-10 level in splenic lymphocyte culture supernatants from the tolerance rats rose markedly (P<0.01). NF-kappaB p65 activity induced by insulin in mesangial cells was inhibited by culture superatants of splenic lymphocytes from oral immune tolerance rats (P<0.05). CONCLUSION: NF-kappaB p65 activity in mesangial cells may be inhibited by IL-10 secreted by splenic lymphocytes from the oral immune tolerance rats.

[Change of activity of NF-kappaB p65 in lymphocytes from rats with oral tolerance induced by Fx1A].

AIM: To explore the activity change and significance of NF-kappaB p65 in lymphocytes from rats with oral tolerance induced by Fx1A. METHODS: 30 female Wistar rats were divided into two groups (oral tolerance and control groups), which stomachs were perfused with Fx1A and PBS, respectively. The delayed-type hypersensitivity (DTH) was evaluated by skin test, the immune function was detected by splenic lymphocyte proliferation test, the activity of NF-kappaB p65 and expression of TGF-beta1 in lymphoid tissues were examined by immunohistochemical staining and Sandwich ELISA. RESULTS: In comparison with control group, the DTH and antigen-specific lymphocyte proliferation reaction in oral tolerance group were suppressed significantly. The activity of NF-kappaB p65 and expression of TGF-beta1 in Peyer's patch were increased notably. However, the activity of NF-kappaB p65 was decreased, but expression of TGF-beta1 was increased markedly in splenic lymphocytes. CONCLUSION: Information of oral tolerance induced by Fx1A may be related to the change of NF-kappaB p65 activity in lymphocytes of body's different places.