The Role of Cytokines Produced via the NLRP3 Inflammasome in Mouse Macrophages Stimulated with Dental Calculus in Osteoclastogenesis.
The Role of Cytokines Produced via the NLRP3 Inflammasome in Mouse Macrophages Stimulated with Dental Calculus in Osteoclastogenesis.
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DOI:
10.3390/ijms222212434
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发表时间:
2021-11-18
影响因子:
5.6
通讯作者:
Yoshimura A
中科院分区:
文献类型:
--
作者:
Mae M;Alam MI;Yamashita Y;Ozaki Y;Higuchi K;Ziauddin SM;Montenegro Raudales JL;Sakai E;Tsukuba T;Yoshimura A
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.
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DOI:
10.1073/pnas.0812690106
发表时间:
2009-06-02
影响因子:
11.1
作者:
Cayrol, Corinne;Girard, Jean-Philippe
通讯作者:
Girard, Jean-Philippe
影响因子:
3.7
作者:
Montenegro Raudales JL;Yoshimura A;Sm Z;Kaneko T;Ozaki Y;Ukai T;Miyazaki T;Latz E;Hara Y
通讯作者:
Hara Y
影响因子:
8.7
作者:
Dinarello CA
通讯作者:
Dinarello CA
影响因子:
3.9
作者:
Fons-Badal, Carla;Fons-Font, Antonio;Agustin-Panadero, Ruben
通讯作者:
Agustin-Panadero, Ruben
影响因子:
4.4
作者:
Kitaura, Hideki;Tatamiya, Mutsuhito;Nakayama, Koji
通讯作者:
Nakayama, Koji