並列タイトル等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
タイトル(掲載誌)International Journal of Molecular Sciences
授与機関名Nagasaki University (長崎大学)
一般注記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)
http://hdl.handle.net/10069/00041434
DOIinfo:doi/10.3390/ijms222212434
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