The Role of Cytokines Produced via the NLRP3 Inflammasome in Mouse Macrophages Stimulated with Dental Calculus in Osteoclastogenesis

• Material Type: 博士論文
• Title: The Role of Cytokines Produced via the NLRP3 Inflammasome in Mouse Macrophages Stimulated with Dental Calculus in Osteoclastogenesis
• Author/Editor: 前, めぐみ
• Author Heading: 前, めぐみ
• Publication, Distribution, etc.: MDPI
• Publication Date: 2022-03-18
• Publication Date (W3CDTF): 2022-03-18
• Alternative Title: 歯石で刺激したマウスマクロファージにおいてNLRP3インフラマソームを介して産生されるサイトカインの破骨細胞形成における役割
• Periodical title: International Journal of Molecular Sciences
• No. or year of volume/issue: 22 22
• Volume: 22
• Issue: 22
• Pages: 12434-
• ISSN (Periodical Title): ISSN : 1422-0067
• Degree grantor/type: Nagasaki University (長崎大学)
• Date Granted: 2022-03-18
• Dissertation Number: 甲医歯薬第1431号
• Degree Type: 博士(歯学)
• Text Language Code: eng
• Subject Heading: dental calculus; NLRP3 inflammasome; IL-1β; IL-18; osteoclast
• Target Audience: 一般
• Note (General): Dental calculus (DC) is a common deposit in periodontitis patients. We have previously shown that DC contains both microbial components and calcium phosphate crystals that induce an osteoclastogenic cytokine IL-1β via the NLRP3 inflammasome in macrophages. In this study, we examined the effects of cytokines produced by mouse macrophages stimulated with DC on osteoclastogenesis. The culture supernatants from wild-type (WT) mouse macrophages stimulated with DC accelerated osteoclastogenesis in RANKL-primed mouse bone marrow macrophages (BMMs), but inhibited osteoclastogenesis in RANKL-primed RAW-D cells. WT, but not NLRP3-deficient, mouse macrophages stimulated with DC produced IL-1β and IL-18 in a dose-dependent manner, indicating the NLRP3 inflammasome-dependent production of IL-1β and IL-18. Both WT and NLRP3-deficient mouse macrophages stimulated with DC produced IL-10, indicating the NLRP3 inflammasome-independent production of IL-10. Recombinant IL-1β accelerated osteoclastogenesis in both RANKL-primed BMMs and RAW-D cells, whereas recombinant IL-18 and IL-10 inhibited osteoclastogenesis. These results indicate that DC induces osteoclastogenic IL-1β in an NLRP3 inflammasome-dependent manner and anti-osteogenic IL-18 and IL-10 dependently and independently of the NLRP3 inflammasome, respectively. DC may promote alveolar bone resorption via IL-1β induction in periodontitis patients, but suppress resorption via IL-18 and IL-10 induction in some circumstances.; 長崎大学学位論文 学位記番号:博(医歯薬)甲第1431号 学位授与年月日:令和4年3月18日; Author: Megumi Mae, Mohammad Ibtehaz Alam, Yasunori Yamashita, Yukio Ozaki, Kanako Higuchi, S.M. Ziauddin, Jorge Luis Montenegro Raudales, Eiko Sakai, Takayuki Tsukuba and Atsutoshi Yoshimura; Citation: International Journal of Molecular Sciences, 22(22), art.no. 12434; 2021; identifier:Nagasaki University (長崎大学), 博士(歯学) (2022-03-18)
• Source: fulltext; https://nagasaki-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=27401&item_no=1&attribute_id=70&file_no=1
• Access Restrictions: インターネット公開
• Rights (production): © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
• Related Material: http://hdl.handle.net/10069/00041434
• Related Material (DOI): 10.3390/ijms222212434
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 長崎大学 : 長崎大学学術研究成果リポジトリ