NMI and IFP35 serve as proinflammatory DAMPs during cellular infection and injury

Zhikai Xiahou, Xiangli Wang, Juan Shen, Xiaoxiao Zhu, Feng Xu, Rong Hu, Deyin Guo, Henan Li, Yong Tian, Yingfang Liu () and Huanhuan Liang ()
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Zhikai Xiahou: Chinese Academy of Sciences
Xiangli Wang: Chinese Academy of Sciences
Juan Shen: Chinese Academy of Sciences
Xiaoxiao Zhu: Chinese Academy of Sciences
Feng Xu: Zhejiang University School of Medicine
Rong Hu: Capital Medical University
Deyin Guo: Sun Yat-Sen University
Henan Li: Peking University People’s Hospital
Yong Tian: Chinese Academy of Sciences
Yingfang Liu: Chinese Academy of Sciences
Huanhuan Liang: Chinese Academy of Sciences

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Damage-associated molecular patterns (DAMP) trigger innate immune response and exacerbate inflammation to combat infection and cellular damage. Identifying DAMPs and revealing their functions are thus of crucial importance. Here we report that two molecules, N-myc and STAT interactor (NMI) and interferon-induced protein 35 (IFP35) act as DAMPs and are released by activated macrophages during lipopolysaccharide-induced septic shock or acetaminophen-induced liver injury. We show that extracellular NMI and IFP35 activate macrophages to release proinflammatory cytokines by activating nuclear factor-κB through the Toll-like receptor 4 pathway. In addition, the serum levels of NMI are increased in patients who succumbed to severe inflammation. NMI deficiency reduces inflammatory responses and mortality in mouse models of sepsis and liver injury. We therefore propose that extracellular NMI and IFP35 exacerbate inflammation as DAMPs, making them potential therapeutic targets for clinical intervention.

Date: 2017
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DOI: 10.1038/s41467-017-00930-9

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