Research Papers:

Inflammasome-independent role of NLRP12 in suppressing colonic inflammation regulated by Blimp-1

Fushan Shi _, Yang Yang, Mohammed Kouadir, Wei Xu, Songhua Hu and Tiancheng Wang

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Oncotarget. 2016; 7:30575-30584. https://doi.org/10.18632/oncotarget.8872

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Fushan Shi1,*, Yang Yang 2,*, Mohammed Kouadir3, Wei Xu4, Songhua Hu4, Tiancheng Wang4

1Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China

2College of Animal Science and Technology, Zhejiang A&F University, Lin’an 311300, China

3Trustchem Co., Ltd., Nanjing 210029, China

4Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China

*These authors contributed equally to this work

Correspondence to:

Fushan Shi, email: [email protected]

Keywords: colitis, inflammation, Blimp-1, NLRP12, TLR4

Received: January 21, 2016     Accepted: March 31, 2016     Published: April 20, 2016


NLRP12 is a member of the Nod-like receptor (NLR). Previous studies have reported enhanced colitis-associated inflammatory responses in NLRP12-deficient mice. In this study, we sought to investigate the role of NLRP12 in DSS-stimulated proinflammatory response in dendritic cells and mice colitis, and the molecular mechanisms involved in the development of the inflammation. Our results showed that down-regulation of NLRP12 is required for DSS-induced release of proinflammatory cytokines IL-1β and TNF-α; that PR domain zinc finger protein 1 (also known as Blimp-1) induces NLRP12 down-regulation during DSS-induced proinflammatory response and colitis; and that TLR4 is implicated in the up-regulation of Blimp-1 that led to the down-regulation of NLRP12 expression in DSS-induced colitis. Taken together, the results suggest that the TLR4-Blimp-1 axis promotes DSS induced experimental colitis through the down-regulation of NLRP12.

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