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B10 Cells Alleviate Periodontal Bone Loss in Experimental Periodontitis.

ABSTRACT: B10 cells can regulate inflammatory responses in innate immunity. Toll-like receptors (TLRs) play an important role in B cell-mediated immune responses in periodontal disease. This study aimed to determine the effects of TLR-activated B10 cells on periodontal bone loss in experimental periodontitis. Spleen B cells isolated from C57BL/6J mice were cultured with Porphyromonas gingivalis lipopolysaccharide (LPS) and cytosine-phospho-guanine (CpG) oligodeoxynucleotides for 48 h. B10-enriched CD1d^hi CD5⁺ B cells were sorted by flow cytometry and were adoptively transferred to recipient mice through tail vein injection. At the same time, P. gingivalis-soaked ligatures were placed subgingivally around the maxillary second molars and remained there for 2 weeks before the mice were euthanized. Interleukin-10 (IL-10) production and the percentage of CD1d^hi CD5⁺ B cells were significantly increased with treatment with P. gingivalis LPS plus CpG compared to those in mice treated with P. gingivalis LPS or CpG alone. Mice with CD1d^hi CD5⁺ B cell transfer demonstrated reduced periodontal bone loss compared to the no-transfer group and the group with CD1d^lo CD5^- B cell transfer. Gingival IL-10 mRNA expression was significantly increased, whereas expressions of receptor activator of NF-?B ligand (RANKL)/osteoprotegerin (OPG), tumor necrosis factor alpha (TNF-?), and IL-1? were significantly inhibited in the CD1d^hi CD5⁺ B cell transfer group. The percentages of CD19⁺ IL-10⁺ cells, CD19⁺ CD1d^hi CD5⁺ cells, and P. gingivalis-binding CD19⁺ cells were significantly higher in recovered mononuclear cells from gingival tissues of the CD1d^hi CD5⁺ B cell transfer group than in tissues of the no-transfer group and the CD1d^lo CD5^- B cell transfer group. This study indicated that the adoptive transfer of B10 cells alleviated periodontal inflammation and bone loss in experimental periodontitis in mice.

SUBMITTER: Wang Y

PROVIDER: S-EPMC5563573 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature

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B10 Cells Alleviate Periodontal Bone Loss in Experimental Periodontitis.

Wang Yuhua Y Yu Xiaoqian X Lin Jiang J Hu Yang Y Zhao Qian Q Kawai Toshihisa T Taubman Martin A MA Han Xiaozhe X

Infection and immunity 20170818 9

B10 cells can regulate inflammatory responses in innate immunity. Toll-like receptors (TLRs) play an important role in B cell-mediated immune responses in periodontal disease. This study aimed to determine the effects of TLR-activated B10 cells on periodontal bone loss in experimental periodontitis. Spleen B cells isolated from C57BL/6J mice were cultured with <i>Porphyromonas gingivalis</i> lipopolysaccharide (LPS) and cytosine-phospho-guanine (CpG) oligodeoxynucleotides for 48 h. B10-enriched ...[more]

PMID: 28652308

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Project description:The present study explored whether the dopamine 2-like receptor agonist, ropinirole, a drug used for treating Parkinson's disease, suppresses neutrophilic inflammation and alveolar bone loss in an experimental rat model of periodontitis. Periodontitis is a neutrophilic inflammatory disease caused by periodontal pathogens. An excessive T helper (Th)17 immune response is involved in the progression of periodontitis, and interleukin (IL)-17 promotes the exacerbation of inflammation and alveolar bone destruction. Recent evidence has suggested that dopamine signaling plays a key role in Th17 cell differentiation, and that dopamine 2-like receptor agonists suppress cytokine production from Th17 cells. We previously demonstrated that tannic acid, which is a dopamine 2-like receptor agonist, inhibits alveolar bone resorption in an experimental model of periodontitis. The present study used a carrageenan-induced rat model of periodontitis with or without ropinirole. Micro-computed tomography analysis was performed. Cells of the murine gingival epithelial cell line GE1 were stimulated with carrageenan and IL-17A in the presence or absence of ropinirole. The anti-inflammatory effect of ropinirole was analyzed using reverse transcription- quantitative PCR and enzyme-linked immunosorbent assay. Subsequently, in the carrageenan-induced rat model of periodontitis, alveolar bone resorption was observed in the maxillary second molar by micro-computed tomography analysis. Intriguingly, ropinirole suppressed the alveolar bone destruction. The expression levels of C-X-C motif chemokine ligand 1 (CXCL1) and IL-17 receptor A (IL-17RA) in GE1 cells were increased by carrageenan, and CXCL1 expression in GE1 cells was upregulated under IL-17A stimulation. Moreover, ropinirole inhibited CXCL1 and IL-17RA expression in GE1 cells in the presence of IL-17A and carrageenan. Finally, haloperidol promoted CXCL1 expression in GE1 cells in the presence of carrageenan. Overall, these findings suggested that ropinirole suppressed neutrophilic inflammation and alveolar bone destruction in periodontitis by inhibiting CXCL1 expression in gingival epithelial cells through the dopamine 2-like receptor. Thus, ropinirole shows promise as a drug for the treatment of periodontitis.

Dataset Information

B10 Cells Alleviate Periodontal Bone Loss in Experimental Periodontitis.

Publications

B10 Cells Alleviate Periodontal Bone Loss in Experimental Periodontitis.

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