TLR2 Elicits IL-17-Mediated RANKL Expression, IL-17, and OPG Production in Neutrophils from Arthritic Mice

Milanova, Viktoriya; Ivanovska, Nina; Dimitrova, Petya

doi:10.1155/2014/643406

Cited by 28 publications

(38 citation statements)

References 44 publications

(54 reference statements)

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“…The Rankl/Opg relative ratio is considered as an accurate diagnostic method for assessing periodontal disease activity . TLR‐2 has been shown to inhibit osteoclastogenesis by downregulating the expression of RANKL . In the present study, we found that the Rankl/Opg mRNA ratio in gingiva was elevated 2 weeks after ligation in peri‐implant tissues in both WT mice and Tlr2‐ KO mice when compared with controls (Figure G).…”

Section: Discussionmentioning

confidence: 92%

Retracted: Role of toll‐like receptor 2 in inflammation and alveolar bone loss in experimental peri‐implantitis versus periodontitis

Hu²,

Freire³

et al. 2017

J of Periodontal Research

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Background and Objective Peri‐implantitis and periodontitis are different entities in immune characteristics even though they share similar features in clinical and radiologic signs. Toll‐like receptor 2 (TLR‐2), one of the key pathogen‐recognition receptors in the innate immune system, plays an important role in the progression of periodontitis. However, the role of TLR‐2 in peri‐implantitis remains unclear. The objective of this study was to investigate the role of TLR‐2 in inflammation and alveolar bone loss in a murine model of ligature‐induced peri‐implantitis and to compare it with ligature‐induced periodontitis. Material and Methods Smooth‐surface titanium implants were placed in the alveolar bone of the left maxillary molars of wild‐type (WT) and Tlr2 knockout (Tlr2‐KO) mice 6 weeks after tooth extraction. Silk ligatures were applied to the left implant fixtures and the right maxillary second molars to induce peri‐implantitis and periodontitis 4 weeks after implant placement. Two weeks after ligation, bone loss around the implants and maxillary second molars was analysed by micro‐computed tomography (micro‐CT), and inflammation around the implants and maxillary second molars was assessed at the same time point using histology and TRAP staining, respectively. Expression of mRNA for proinflammatory cytokines (interleukin‐1β [Il1β], tumor necrosis factor‐α [Tnfα]), an anti‐inflammatory cytokine (interleukin‐10 [Il10]) and osteoclastogenesis‐related cytokines (Rankl, osteoprotegerin [Opg]) were evaluated, in gingival tissue, using real‐time quantitative PCR (RT‐qPCR). Results The success rate of implant osseointegration was significantly higher in Tlr2‐KO mice (85.71%) compared with WT mice (53.66%) (P = .0125). Micro‐CT revealed significantly decreased bone loss in Tlr2‐KO mice compared with WT mice (P = .0094) in peri‐implantitis. The levels of mRNA for Il1β (P = .0055), Tnfα (P = .01) and Il10 (P = .0019) in gingiva were significantly elevated in the peri‐implantitis tissues of WT mice, but not in Tlr2‐KO mice, compared with controls. However, the gingival mRNA ratios of Rankl/Opg in peri‐implant tissues were significantly upregulated in both WT (P = .0488) and Tlr2‐KO (P = .0314) mice. Ligature‐induced periodontitis exhibited similar patterns of bone loss and inflammatory cytokine profile in both groups of mice, except that the level of Il10 was elevated (P = .0114) whereas the Rankl/Opg ratio was not elevated (P = .9755) in Tlr2‐KO mice compared with control mice. Histological findings showed increased numbers of TRAP‐positive cells and infiltrated inflammatory cells in ligature‐induced peri‐implantitis in both WT (P < .01) and Tlr2‐KO mice (P < .05), and the numbers of both types of cell were significantly higher in WT mice than in Tlr2‐KO mice (P < .01). Conclusion This study suggests that TLR‐2 mediates bone loss in both peri‐implantitis and periodontitis. However, different molecular features may exist in the pathogenesis of the two diseases.

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Section: Discussionmentioning

confidence: 92%

Retracted: Role of toll‐like receptor 2 in inflammation and alveolar bone loss in experimental peri‐implantitis versus periodontitis

Hu²,

Freire³

et al. 2017

J of Periodontal Research

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“…55 Neutrophils in the circulation of arthritic mice spontaneously produce IL-17 in vitro. 56 IL-17 produced by neutrophils also participates in inflammation-induced airway neutrophilia. 20 Higher levels of IL17 + CD177 + neutrophils in the peripheral blood in allergic asthma patients might contribute to disease progression.…”

Section: Discussionmentioning

confidence: 99%

Characterization and biological significance of IL-23-induced neutrophil polarization

et al. 2017

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Neutrophils are heterogeneous with distinct subsets, and can switch phenotypes to exert regulatory functions on immunity. We herein demonstrate that IL-23-treated neutrophils selectively produce IL-17A, IL-17F and IL-22, and display a distinct gene expression profile in contrast to resting and lipopolysaccharide-treated neutrophils. IL-17 neutrophils are present in the colons of mice with dextran sulfate sodium-induced colitis. Adoptive transfer of IL-23-treated neutrophils significantly promotes pathogenesis in this model. IL-23 induces neutrophil polarization through STAT3-dependent RORγt and BATF pathways. Thus, IL-23-induced neutrophil polarization expresses a unique cytokine-producing profile, which may contribute to IL-23-mediated inflammatory diseases.

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“…For example, activated Th17 cells are involved in the induction of inflammation by stimulating neutrophils, causing their chemoattraction into the joints. [22][23][24] Furthermore, neutrophils play a crucial role in the activation of NK cells, as their depletion has led to impairment in the function and homeostasis of NK cells. 25…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

<p>Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis</p>

Elemam¹,

Hannawi

Maghazachi³

2020

ITT

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Rheumatoid arthritis (RA) is one of the most prevalent autoimmune diseases and a prototypic inflammatory disease, affecting the small joints of the hands and feet. Chemokines and chemokine receptors play a critical role in RA pathogenesis via immune cells recruitment. Several chemokines and chemokine receptors are abundant in the peripheral blood and in the local inflamed joints of RA. Furthermore, synthetic and biologics disease modifying anti rheumatic drugs have been reported to affect chemokines expression. Thus, many studies have focused on targeting chemokines and chemokine receptors, where some have shown positive promising results. However, most of the chemokine blockers in human trials of RA treatment displayed some failures that can be attributed to several reasons in their structures and binding affinities. Nevertheless, targeting chemokines will continue to be under development, in order to improve their therapeutic potentials in RA and other autoimmune diseases. In this review we provide an up-to-date knowledge regarding the role of chemokines and chemokine receptors in RA with an emphasis on their activities on immune cells. We also discussed the effects of drugs targeting those molecules in RA. This knowledge might provide impetus for developing new therapeutic modalities to treat this chronic disease.

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TLR2 Elicits IL-17-Mediated RANKL Expression, IL-17, and OPG Production in Neutrophils from Arthritic Mice

Cited by 28 publications

References 44 publications

Retracted: Role of toll‐like receptor 2 in inflammation and alveolar bone loss in experimental peri‐implantitis versus periodontitis

Retracted: Role of toll‐like receptor 2 in inflammation and alveolar bone loss in experimental peri‐implantitis versus periodontitis

Characterization and biological significance of IL-23-induced neutrophil polarization

<p>Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis</p>

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