Local promotion of B cells (B10) function alleviates experimental periodontitis bone loss through antagonizing Receptor Activator of NF‐KappaB Ligand‐expressing neutrophils

2020 ◽  
Author(s):  
Guoqin Cao ◽  
Xu Zhang ◽  
Yuqi Song ◽  
Yi Sun ◽  
Hong Ling ◽  
...  
Keyword(s):  
B Cells ◽  
Bone Loss ◽  
Receptor Activator ◽  
Experimental Periodontitis ◽  
Nf Kappab

scholarly journals B10 Cells Alleviate Periodontal Bone Loss in Experimental Periodontitis

2017 ◽  
Vol 85 (9) ◽  
Author(s):  
Yuhua Wang ◽  
Xiaoqian Yu ◽  
Jiang Lin ◽  
Yang Hu ◽  
Qian Zhao ◽  
...  
Keyword(s):  
B Cells ◽  
Bone Loss ◽  
B Cell ◽  
Cell Transfer ◽  
Content Type ◽  
Periodontal Inflammation ◽  
Periodontal Bone Loss ◽  
Experimental Periodontitis ◽  
Transfer Group ◽  
B10 Cells

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 CD1dhi 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 CD1dhi 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 CD1dhi CD5+ B cell transfer demonstrated reduced periodontal bone loss compared to the no-transfer group and the group with CD1dlo CD5− B cell transfer. Gingival IL-10 mRNA expression was significantly increased, whereas expressions of receptor activator of NF-κB ligand (RANKL)/osteoprotegerin (OPG), tumor necrosis factor alpha (TNF-α), and IL-1β were significantly inhibited in the CD1dhi CD5+ B cell transfer group. The percentages of CD19+ IL-10+ cells, CD19+ CD1dhi CD5+ cells, and P. gingivalis-binding CD19+ cells were significantly higher in recovered mononuclear cells from gingival tissues of the CD1dhi CD5+ B cell transfer group than in tissues of the no-transfer group and the CD1dlo 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.

scholarly journals TREM-1 Is Upregulated in Experimental Periodontitis, and Its Blockade Inhibits IL-17A and RANKL Expression and Suppresses Bone loss

2019 ◽  
Vol 8 (10) ◽  
pp. 1579 ◽  
Author(s):  
Nagihan Bostanci ◽  
Toshiharu Abe ◽  
Georgios N. Belibasakis ◽  
George Hajishengallis
Keyword(s):  
Bone Loss ◽  
Clinical Evidence ◽  
Bacterial Load ◽  
Underlying Mechanism ◽  
Receptor Activator ◽  
Molar Teeth ◽  
Experimental Periodontitis ◽  
The Impact ◽  
First Time

Aim: Triggering receptor expressed on myeloid cells-1 (TREM-1) is a modifier of local and systemic inflammation. There is clinical evidence implicating TREM-1 in the pathogenesis of periodontitis. However, a cause-and-effect relationship has yet to be demonstrated, as is the underlying mechanism. The aim of this study was to elucidate the role of TREM-1 using the murine ligature-induced periodontitis model. Methods: A synthetic antagonistic LP17 peptide or sham control was microinjected locally into the palatal gingiva of the ligated molar teeth. Results: Mice treated with the LP17 inhibitor developed significantly less bone loss as compared to sham-treated mice, although there were no differences in total bacterial load on the ligatures. To elucidate the impact of LP17 on the host response, we analyzed the expression of a number of immune-modulating genes. The LP17 peptide altered the expression of 27/92 genes ≥ two-fold, but only interleukin (IL)-17A was significantly downregulated (4.9-fold). Importantly, LP17 also significantly downregulated the receptor activator of nuclear factor kappa-B-ligand (RANKL) to osteoprotegerin (OPG) ratio that drives osteoclastic bone resorption in periodontitis. Conclusion: Our findings show for the first time that TREM-1 regulates the IL-17A-RANKL/OPG axis and bone loss in experimental periodontitis, and its therapeutic blockade may pave the way to a novel treatment for human periodontitis.

scholarly journals Local Induction of B Cell Interleukin-10 Competency Alleviates Inflammation and Bone Loss in Ligature-Induced Experimental Periodontitis in Mice

2016 ◽  
Vol 85 (1) ◽  
Author(s):  
Pei Yu ◽  
Yang Hu ◽  
Zhiqiang Liu ◽  
Toshihisa Kawai ◽  
Martin A. Taubman ◽  
...  
Keyword(s):  
B Cells ◽  
Bone Loss ◽  
Critical Role ◽  
Cell Activity ◽  
Interleukin 10 ◽  
Tartrate Resistant Acid Phosphatase ◽  
Periodontal Inflammation ◽  
Experimental Periodontitis

ABSTRACT Interleukin-10 (IL-10)-producing B cells (B10 cells) play a critical role in the immune system balance by negatively regulating inflammatory responses. This study was conducted to determine the effect of local B10 cell induction on periodontal inflammation and bone loss in ligature-induced experimental periodontitis in vivo. Purified spleen B cells from C57BL/6J mice (8 to 10 weeks old) were cultured with CD40 ligand (CD40L) and the Toll-like receptor 9 (TLR9) agonist cytidine-phosphate-guanosine oligodeoxynucleotide (CpG) to determine effective IL-10 induction in vitro. Silk ligatures (size 7-0) were tied around the mouse maxillary second molars on day 0, followed by the injection of CD40L and CpG into the palatal gingiva on days 3, 6, and 9. All the mice were sacrificed, and samples were collected on day 14. CD40L and CpG significantly increased the level of IL-10 production by B cells in vitro, although the frequencies of CD1dhi CD5+ and IL-10-producing (IL-10+) CD45+ cells were decreased. IL-10 was predominantly produced by the CD1dhi CD5+ subpopulation of B cells. In vivo, both IL-10 mRNA expression and the number of IL-10+ CD45+ cells were significantly increased after gingival injection of CD40L and CpG. Periodontal bone loss was significantly decreased and the gingival expression of IL-1β, tumor necrosis factor alpha, and RANKL was significantly reduced. The number of multinucleated tartrate-resistant acid phosphatase-positive cells along the alveolar bone surface was significantly decreased after gingival injection of CD40L and CpG. This study indicates for the first time that the local induction of B10 cell activity could inhibit periodontal inflammation and bone loss.

scholarly journals RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

2016 ◽  
Vol 291 (48) ◽  
pp. 24838-24850 ◽  
Author(s):  
Yuko Fujiwara ◽  
Marilina Piemontese ◽  
Yu Liu ◽  
Jeff D. Thostenson ◽  
Jinhu Xiong ◽  
...  
Keyword(s):  
B Cells ◽  
Bone Loss ◽  
Estrogen Deficiency ◽  
Receptor Activator

3,4,5-Trihydroxybenzoic acid attenuates ligature-induced periodontal disease in Wistar rats.

2020 ◽  
Vol 19 ◽  
Author(s):  
Ozkan Karatas ◽  
Fikret Gevrek
Keyword(s):  
Bone Loss ◽  
Gallic Acid ◽  
Wistar Rats ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Collagenase Activity ◽  
Osteoblastic Activity ◽  
Cell Counts ◽  
Experimental Periodontitis ◽  
Anti Inflammatory

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.

Mouse model of experimental periodontitis induced byPorphyromonas gingivalis/Fusobacterium nucleatuminfection: bone loss and host response

2009 ◽  
Vol 36 (5) ◽  
pp. 406-410 ◽  
Author(s):  
David Polak ◽  
Asaf Wilensky ◽  
Lior Shapira ◽  
Amal Halabi ◽  
Dita Goldstein ◽  
...  
Keyword(s):  
Bone Loss ◽  
Mouse Model ◽  
Host Response ◽  
Experimental Periodontitis
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