Interleukin-10 Deficiency Increases Kidney Inflammation And Fibrosis In Mouse Ischemia-reperfusion Injury Model

Aims:As the final common pathway leading to end-stage renal disease(ESRD),renal tubulointerstitial fibrosis exist in various types of renal diseases and its severity correlates strongly with the inflammatory status.IL-10 also has key roles in suppressing inflammatory processes,mainly through blocking activation of inflammatory pathways and inhibiting the secretion of pro-inflammatory mediators.This study is to further explore the role of IL-10 in the progression of AKI to CKD and provides a new theoretical basis for its prevention and treatment.Methods:12 IL-10-/-mice(KO)aged 8-10 weeks and 12 C57BL/6 wild type mice(WT)aged 8-10 weeks were divided into control group(Sham)and renal IR group(IR).Hematoxylin and eosin(HE)staining and Masson staining were used to observe the renal tissue morphology change;Immunohistochemical detection of IL-6,IL-18,Ki67 and TGF-?1 expression;Western blotting to detect the expression of IL-6,IL-18 and TGF-beta1.Results:Compared with Sham group and WT IR group,KO group mouse renal pathological damage was more severe,proinflammatory factor IL-6 and IL-18 shows higher expression(P<0.01).Renal interstitial fibrosis was visible,renal tubular epithelial cells Ki67 expression decreased distinctly(P<0.01),the expression of TGF-beta1 increased significantly(P<0.01).Conclusion:Our study demonstrates that repair slows down significantly after kidney ischemia-reperfusion injury and fibrosis occurs gradually in IL-10-/-mice,eventually progressing to chronic kidney disease.