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

Autor: Mohammad Ibtehaz Alam, Takayuki Tsukuba, Eiko Sakai, Jorge Luis Montenegro Raudales, Yukio Ozaki, Yasunori Yamashita, S.M. Ziauddin, Atsutoshi Yoshimura, Megumi Mae, Kanako Higuchi
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Inflammasomes
medicine.medical_treatment
Interleukin-1beta
Alveolar Bone Loss
Osteoclasts
law.invention
Mice
law
Osteogenesis
Biology (General)
Spectroscopy
Mice
Knockout
integumentary system
Chemistry
Interleukin-18
Inflammasome
General Medicine
Computer Science Applications
Resorption
Cell biology
Interleukin-10
Cytokine
medicine.anatomical_structure
IL-1β
osteoclast
Recombinant DNA
Interleukin 18
IL-18
medicine.drug
Signal Transduction
QH301-705.5
Primary Cell Culture
Catalysis
Article
Cell Line
Inorganic Chemistry
Osteoclast
NLR Family
Pyrin Domain-Containing 3 Protein
medicine
Animals
Humans
Physical and Theoretical Chemistry
Periodontitis
Molecular Biology
QD1-999
Macrophages
Organic Chemistry
RANK Ligand
dental calculus
Macrophage Activation
medicine.disease
NLRP3 inflammasome
Disease Models
Animal
Gene Expression Regulation
Culture Media
Conditioned
Bone marrow
Zdroj: International Journal of Molecular Sciences
Volume 22
Issue 22
International Journal of Molecular Sciences, Vol 22, Iss 12434, p 12434 (2021)
ISSN: 1422-0067
Popis: 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.
International Journal of Molecular Sciences, 22(22), art. no. 12434; 2021
Databáze: OpenAIRE
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