Toll-like receptor agonists Porphyromonas gingivalis LPS and CpG differentially regulate IL-10 competency and frequencies of mouse B10 cells

Liu, Zhiqiang; Hu, Yang; Yu, Pei; Ma, Lin; Huang, Grace; Kawai, Toshihisa; Taubman, Martin A.; Wang, Zuomin; Han, Xiaozhe

doi:10.1590/1678-77572016-0277

Cited by 10 publications

(9 citation statements)

References 27 publications

(34 reference statements)

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“…Thus, the ideal osteoimmunological treatment for peri-implantitis should include both direct antiosteoclastogenesis and anti-inflammation components. As innate immune recognition receptors, TLR family plays a central role in innate immunity, inflammation, cell survival, and proliferation [5,26,37,38]. TLR2 and TLR4 Fig.…”

Section: Discussionmentioning

confidence: 99%

RANKL blockade alleviates peri-implant bone loss and is enhanced by anti-inflammatory microRNA-146a through TLR2/4 signaling

Pan

Hu²,

Wang³

et al. 2020

Int J Implant Dent

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Background: The present study was to determine the effect of local anti-RANKL antibody administration in the presence or absence of microRNA-146a on ligature-induced peri-implant bone resorption, and the potential role of TLR2/4 signaling in such effect.Results: Titanium implants were placed in the left maxilla alveolar bone 6 weeks after extraction of first and second molars in C57/BL6 wild-type (WT) and TLR2 −/− TLR4 −/− (TLR2/4 KO) mice. Silk ligatures were tied around the implants 4 weeks after implantation. Anti-RANKL antibody (500 μg/mL) with or without microRNA 146a (miR-146a) (100 nM) was injected into palatal gingiva around implant on days 3, 6, and 9 during 2 weeks of ligation period. Bone resorption around the implants was assessed by 2D imaging using area measurement and 3D imaging using micro-computed tomography (μCT). Real-time quantitative PCR (RT-qPCR) was used to determine the peri-implant gingival mRNA expression levels of pro-inflammatory cytokines (TNF-α) and osteoclastogenesis-related cytokines (RANKL). In both WT and TLR2/4 KO mice, the bone resorption around implants was significantly increased in the ligation only group when compared to the non-ligation group, but TLR2/4 KO mice showed significantly less bone loss compared to WT mice after ligation. As expected, gingival injection of anti-RANKL antibody significantly reduced bone loss compared with the ligation only group in both WT and TLR2/4 KO mice. Moreover, injection of miR-146a in addition to anti-RANKL antibody significantly enhanced the inhibition of bone loss in WT mice but not in TLR2/4 KO mice. Gingival mRNA expressions of RANKL were significantly reduced by anti-RANKL antibody treatment in both WT and TLR2/4 KO mice but were not affected by the additional miR-146a treatment. Gingival mRNA expression of TNF-α was significantly reduced by miR-146a treatment in WT mice but not in TLR2/4 KO mice. The number of gingival inflammatory cell infiltration and peri-implant TRAP-positive cell formation was significantly reduced by the additional miR-146a treatment in WT mice but not in TLR2/4 KO mice.Conclusions: This study suggests that anti-inflammatory miR-146a enhance anti-RANKL-induced inhibition of periimplant bone resorption through the regulation of TLR2/4 signaling and inhibition of TNF-α expression.

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Section: Discussionmentioning

confidence: 99%

RANKL blockade alleviates peri-implant bone loss and is enhanced by anti-inflammatory microRNA-146a through TLR2/4 signaling

Pan

Hu²,

Wang³

et al. 2020

Int J Implant Dent

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“…There are several approaches to induction of IL‐10 expression in B cells. One of them is that exposure to LPS in the culture or in vivo . Because LPS was eliminated from EBI during preparation, it is clear that the effects of EBI on induction of IL‐10 expression in B cells is not through LPS.…”

Section: Discussionmentioning

confidence: 99%

Probiotic extracts ameliorate nasal allergy by inducing interleukin‐35‒producing dendritic cells in mice

Xue

et al. 2019

Int Forum Allergy Rhinol

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Background:The therapeutic efficacy of allergic rhinitis (AR) needs to be improved. Probiotics have immunoregulatory functions. In this study we evaluated the effects of protein extracts of probiotics in the amelioration of AR.Methods: Extracts of Bifidobacterium infantis (EBI) were prepared by lysing the live probiotics. AR mice were developed to be used to evaluate the therapeutic efficacy of EBI. Results:The results show that EBI induced interleukin (IL)-10-producing dendritic cells (DCs) via increasing IL-35 and signal transducer and activator of transcription 3 (STAT3) phosphorylation. IL-10-expressing DCs induced IL-10-producing B cells (B10 cells), with the la er showing immunosuppressive functions. A er challenge with specific antigens, AR mice showed sneezing, nasal itch, and increases in serum-specific immunoglobulin E (IgE) and mouse mast cell protease-1; higher levels of T helper 2 (Th2) cytokines (IL-4, 67.17 ± 10.66; IL-5, 62.83 ± 9.70; IL-13, 51.00 ± 6.69, before treatment) in nasal mucosal protein extracts, which were significantly suppressed (IL-4, 27.00 ± 6.66; 23.86 ± 4.53;25.67 ± 4.93, a er treatment (p < 0.001) by administration with EBI nasal drops.Conclusion: EBI can suppress AR via inducing B10 cells. Thus, a er carrying out required preclinical experiments and tests, EBI has the translational potential to be used in the treatment of AR and other allergic diseases. C 2019 ARS-AAOA, LLC. How to Cite this Article:Xue J-M, Ma F, An Y-F, et al. Probiotic extracts ameliorate nasal allergy by inducing interleukin-35-producing dendritic cells in mice. Int Forum Allergy Rhinol. 2019;9: 1289-1296.A llergy (AR) is an adverse response to food antigens by the immune system in the airway mucosa. The under-

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“…292 Immunized B cells secreted elevated interleukin-10 levels, compared with nonimmunized B cells. 292 Based on these in vitro findings, further studies characterized regulatory B cells in rodent experimental periodontitis models. Hu et al used the rat ligature-induced periodontal disease model, with or without local CD40 ligand injections into the palatal gingiva.…”

Section: B Cellsmentioning

confidence: 93%

“…277 In contrast, Demoersman et al reported that B1 cells are diminished in peripheral blood of periodontitis patients compared with healthy patients. 286 Timely reports have characterized regulatory B cells to play a critical role in suppressing inflammatory responses in vitro 292,293 and ameliorating alveolar bone loss in vivo. [293][294][295] Liu et al performed an in vitro study in which isolated splenic B cells were immunized with P. gingivalis and treated with CD40 ligand and CpG to induce B cell-derived toll-like receptor signaling.…”

Section: B Cellsmentioning

confidence: 99%

Maintaining homeostatic control of periodontal bone tissue

Hathaway‐Schrader

Novince

2021

Periodontology 2000

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Alveolar bone is a unique osseous tissue due to the integration of the teeth and the proximity of dental plaque biofilms. Periodontal health and homeostasis are mediated by a balanced host immune response to polymicrobial oral biofilms. Shifts in the composition and quantity of microbes within dental plaque biofilms can drive a local proinflammatory immune response state in the epithelial and gingival barrier connective tissues. Infiltrating proinflammatory immune cells within the inflamed connective tissue secrete local factors that induce paracrine signaling to subjacent bone cells.Sustained chronic inflammation disrupts "coupled" osteoclast-osteoblast actions, which ultimately result in alveolar bone destruction. This chapter will provide an overview of alveolar bone physiology and will highlight why the oral microbiota is a critical regulator of alveolar bone remodeling. The ecology of subgingival plaque biofilms will be reviewed considering our understanding that periodontitis is a polymicrobial disruption of host homeostasis. The pathogenesis of periodontal bone loss will be explained from both a historical and current perspective, providing the opportunity to revisit the role of fibrosis in alveolar bone destruction. The molecular basis of host-microbe interactions will be discussed in the context of the commensal oral flora in periodontal health and pathogenic shifts in the oral microbiota during periodontal disease states. The role of periodontal innate and adaptive immune cell interactions with bone cells will be reviewed based on our current understanding of osteoimmunological mechanisms influencing alveolar bone remodeling. Lastly, probiotic/prebiotic therapeutic interventions in the oral microbiota will be evaluated as a potential therapy to support alveolar bone homeostasis/ prevent periodontal bone loss.

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Toll-like receptor agonists Porphyromonas gingivalis LPS and CpG differentially regulate IL-10 competency and frequencies of mouse B10 cells

Cited by 10 publications

References 27 publications

RANKL blockade alleviates peri-implant bone loss and is enhanced by anti-inflammatory microRNA-146a through TLR2/4 signaling

RANKL blockade alleviates peri-implant bone loss and is enhanced by anti-inflammatory microRNA-146a through TLR2/4 signaling

Probiotic extracts ameliorate nasal allergy by inducing interleukin‐35‒producing dendritic cells in mice

Maintaining homeostatic control of periodontal bone tissue

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