Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages.

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ID: 70638
2019
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Abstract
Nickel (Ni), an environmental hazard, widely causes allergic contact hypersensitivity worldwide. Despite that Ni-stimulated pro-inflammatory response is vital in allergy, the underlying molecular mechanisms remain largely unclear. Here, we demonstrated that NiCl activated nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPKs) and interferon regulatory factor 3 (IRF3) signaling pathways in primary bone marrow-derived macrophages (BMDMs), leading to the altered transcription levels of interleukin-1β (IL-1β), -6, -8, -18, tumor necrosis factor-α (TNF-α) and interferon β (INF-β). We also found that nickel chloride (NiCl) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1β. NiCl induced the accumulation of mitochondrial reactive oxygen species (mtROS) and the release of mitochondrial DNA (mtDNA), thus activating NLRP3 inflammasome pathway. Additionally, NiCl-induced apoptosis was dependent on the generation of mtROS, and caspase-1 activation might also partly contribute to the apoptotic process. Altogether, abovementioned results indicate that NiCl induces inflammatory activation in BMDMs via NF-κB, MAPKs, IRF3 signaling pathways as well as NLRP3 inflammasome pathway, which provides a mechanism to improve the efficiency of treatment against Ni-induced allergic reactions.
Reference Key
guo2019nickelaging Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Guo, Hongrui;Liu, Huan;Jian, Zhijie;Cui, Hengmin;Fang, Jing;Zuo, Zhicai;Deng, Junliang;Li, Yinglun;Wang, Xun;Zhao, Ling;Geng, Yi;Ouyang, Ping;Lai, Weiming;Chen, Zhengli;Huang, Chao;
Journal Aging
Year 2019
DOI
10.18632/aging.102570
URL
Keywords
apoptosis inflammasome nf-κb bmdms nicl2

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