| First Author | Mae M | Year | 2021 |
| Journal | Int J Mol Sci | Volume | 22 |
| Issue | 22 | PubMed ID | 34830316 |
| Mgi Jnum | J:320974 | Mgi Id | MGI:6828184 |
| Doi | 10.3390/ijms222212434 | Citation | Mae M, et al. (2021) The Role of Cytokines Produced via the NLRP3 Inflammasome in Mouse Macrophages Stimulated with Dental Calculus in Osteoclastogenesis. Int J Mol Sci 22(22) |
| abstractText | 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-1beta 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-1beta and IL-18 in a dose-dependent manner, indicating the NLRP3 inflammasome-dependent production of IL-1beta 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-1beta 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-1beta 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-1beta induction in periodontitis patients, but suppress resorption via IL-18 and IL-10 induction in some circumstances. |
