Nur77 deficiency leads to systemic inflammation in elderly mice

Journal of Inflammation

Short Report

Xiu-Ming Li¹  Shen Zhang¹  Jian-Ming Li¹  Qian Xu¹  Xing-Xing Lu¹  Peng-Da Guo¹  Hua Wu¹  Jing-Ru Wang¹ 

[1] Pathology Center and Department of Pathology, Soochow University, 215123, Suzhou, China;

关键词: Nur77;    Inflammation;    Immunity;    Animal study;   

DOI  :  10.1186/s12950-015-0085-0

 received in 2015-04-18, accepted in 2015-06-18,  发布年份 2015

来源: Springer

【 摘 要 】

Background Nur77, an orphan member of the nuclear receptor superfamily, has been implicated in the regulation of inflammation. However, the in vivo function of Nur77 remains largely unexplored. In the current study, we investigated the role of Nur77 in inflammation and immunity in mice.FindingsWe found that elderly 8-month-old Nur77-deficient mice (Nur77−/−) developed systemic inflammation. Compared to wild-type (WT) mice (Nur77+/+), Nur77−/− mice showed splenomegaly, severe infiltration of inflammatory cells in several organs including liver, lung, spleen and kidney, increased hyperplasia of fibrous tissue in the lung and enlargement of kidney glomeruli. Additionally, Nur77−/− mice had increased production of pro-inflammatory cytokines and immunoglobulin, and elicited pro-inflammatory M1-like polarization in macrophages as revealed by increased expression of CXCL11 and INDO, and decreased expression of MRC1.ConclusionsThese in vivo observations provide evidence for a pivotal role for Nur77 in the regulation of systemic inflammation and emphasize the pathogenic significance of Nur77 in vivo.

【 授权许可】

Unknown   
© Li et al. 2015. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.