在输尿管梗阻诱导的慢性肾病野生型和NOD1/NOD2双敲除小鼠之间，肾损伤和纤维化无差异。
No difference in renal injury and fibrosis between wild-type and NOD1/NOD2 double knockout mice with chronic kidney disease induced by ureteral obstruction.
作者信息
Stroo Ingrid, Emal Diba, Butter Loes M, Teske Gwen J, Claessen Nike, Dessing Mark C, Girardin Stephen E, Florquin Sandrine, Leemans Jaklien C
机构信息
Department of Pathology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, room L2-112, 1105, AZ, Amsterdam, The Netherlands.
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
出版信息
BMC Nephrol. 2018 Apr 2;19(1):78. doi: 10.1186/s12882-018-0867-8.
BACKGROUND
Chronic kidney disease (CKD) is characterized by sustained tissue damage and ongoing tubulo-interstitial inflammation and fibrosis. Pattern recognition receptors (PRRs) including Toll-like receptors (TLRs) and NOD-like receptors (NLRs) can sense endogenous ligands released upon tissue damage, leading to sterile inflammation and eventually irreversible kidney disease. It is known that NOD1 and NOD2 contribute to the pathogenesis of various inflammatory diseases, including acute kidney injury. However their role in chronic kidney disease is largely unknown. The aim of this study was therefore to investigate the contribution of NOD1 and NOD2 in renal interstitial fibrosis and obstructive nephropathy.
METHODS
To do so, we performed unilateral ureteral obstruction (UUO) in wild type (WT) and NOD1/NOD2 double deficient (DKO) mice and analysed renal damage, fibrosis and inflammation. Data were analysed using the non-parametric Mann-Whitney U-test.
RESULTS
Minor changes in inflammatory response were observed in NOD1/2 DKO mice, while no effects were observed on renal injury and the development of fibrosis.
CONCLUSION
No difference in renal injury and fibrosis between WT and NOD1/NOD2 DKO mice following obstructive nephropathy induced by ureteral obstruction.
背景
慢性肾脏病（CKD）的特征是持续的组织损伤以及肾小管间质炎症和纤维化。包括Toll样受体（TLR）和NOD样受体（NLR）在内的模式识别受体（PRR）能够感知组织损伤时释放的内源性配体，从而引发无菌性炎症并最终导致不可逆的肾脏疾病。已知NOD1和NOD2参与包括急性肾损伤在内的各种炎症性疾病的发病机制。然而，它们在慢性肾脏病中的作用在很大程度上尚不清楚。因此，本研究的目的是探究NOD1和NOD2在肾间质纤维化和梗阻性肾病中的作用。
方法
为此，我们在野生型（WT）小鼠和NOD1/NOD2双缺陷（DKO）小鼠中进行了单侧输尿管梗阻（UUO），并分析了肾脏损伤、纤维化和炎症情况。数据采用非参数Mann-Whitney U检验进行分析。
结果
在NOD1/2 DKO小鼠中观察到炎症反应有轻微变化，而在肾损伤和纤维化发展方面未观察到影响。
结论
输尿管梗阻诱导的梗阻性肾病后，WT小鼠和NOD1/NOD2 DKO小鼠在肾损伤和纤维化方面无差异。
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