Volume 47, Issue 4 pp. 451-460
PRE-CLINICAL SCIENCES

NLRP3 inflammasome mediates M1 macrophage polarization and IL-1β production in inflammatory root resorption

Jie Zhang

Jie Zhang

Department of Orthodontics, The Affiliated Hospital of Qingdao University, Qingdao, China

School of Stomatology, Qingdao University, Qingdao, China

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Xinqiang Liu

Xinqiang Liu

Department of Orthodontics, The Affiliated Hospital of Qingdao University, Qingdao, China

School of Stomatology, Qingdao University, Qingdao, China

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Chunyan Wan

Chunyan Wan

School of Stomatology, Qingdao University, Qingdao, China

Department of Endodontics, The Affiliated Hospital of Qingdao University, Qingdao, China

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Yang Liu

Yang Liu

Department of Orthodontics, The Affiliated Hospital of Qingdao University, Qingdao, China

School of Stomatology, Qingdao University, Qingdao, China

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Yaqi Wang

Yaqi Wang

Department of Orthodontics, The Affiliated Hospital of Qingdao University, Qingdao, China

School of Stomatology, Qingdao University, Qingdao, China

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Chenda Meng

Chenda Meng

School of Stomatology, Qingdao University, Qingdao, China

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Yipeng Zhang

Yipeng Zhang

School of Stomatology, Qingdao University, Qingdao, China

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Chunmiao Jiang

Corresponding Author

Chunmiao Jiang

Department of Orthodontics, The Affiliated Hospital of Qingdao University, Qingdao, China

School of Stomatology, Qingdao University, Qingdao, China

Correspondence

Chunmiao Jiang, Department of Orthodontics, The Affiliated Hospital of Qingdao University, #16 Jiangsu Road, Qingdao, China.

Email: [email protected]

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First published: 24 January 2020
Citations: 179
Jie Zhang and Xinqiang Liu are co-first authors and contributed equally to this work.

Abstract

Aims

To explore the involvement of NOD-like receptor protein 3 (NLRP3) inflammasome and M1 macrophage in root resorption (RR).

Methods

A rat RR model was established by excessive orthodontic force. After different force-loading time, the expression levels of NLRP3, caspase-1, and interleukin-1β (IL-1β) and distribution of M1 macrophages were analysed by immunohistochemistry and immunofluorescence staining in vivo. Then, the mechanism of NLRP3 activation was further verified by macrophage and human periodontal ligament cell (hPDLC) co-culture system in vitro. The production levels of NLRP3, caspase-1, pro-caspase-1, and IL-1β in M1 macrophages in the co-culture system were detected by Western blot, and the polarization of CD68+IL-1β+ M1 macrophages was detected by immunofluorescence staining.

Results

In the rat RR model, NLRP3, caspase-1, IL-1β, and M1 macrophages were expressed in periodontal ligament, mainly concentrated around RR areas. Force-pre-treated hPDLCs promoted M1 macrophage polarization and the production of NLRP3, caspase-1, and IL-1β in M1 macrophages in co-culture system. When MCC950, an inhibitor of NLRP3 inflammasome, was added, NLRP3 activation and M1 macrophage polarization were inhibited.

Conclusions

In periodontal tissues, hPDLCs stimulated by force promoted M1 macrophage polarization and increased IL-1β production by activating NLRP3 inflammasome in M1 macrophages, thus initiating the occurrence of RR.

CONFLICT OF INTEREST

The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.

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