Advanced glycation end‐products and <i>Porphyromonas gingivalis</i> lipopolysaccharide increase calprotectin expression in human gingival epithelial cells

Hiroshima, Yuka; Sakamoto, Eijiro; Yoshida, Kaya; Abe, Kaori; Naruishi, Koji; Yamamoto, Toshiharu; Shinohara, Yasuo; Kido, Jun‐ichi; Geczy, Carolyn L.

doi:10.1002/jcb.26319

Cited by 25 publications

(24 citation statements)

References 42 publications

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“…Furthermore, in the same study, with stimulation of AGE and/or P-LPS, the CLP complex was expressed not only in the cytoplasm but also in the nucleus. This result suggests that CLP might inhibit the growth of accelerated cells mediated by AGE and/or P-LPS by supporting repair of damaged tissues, thus maintaining the function of gingival epithelial barrier to resist infection and inflammation [87]. The findings mentioned above suggest that released CLP may act on periodontopathic bacteria in the presence of neutrophils and monocytes, but in the case of epithelial and keratinocytes, intracellular CLP may act on bacteria invading gingival epithelium.…”

Section: The Role Of Clp In Pdmentioning

confidence: 99%

Role of Calprotectin as a Biomarker in Periodontal Disease

Wei

Liu

Xiong

2019

Mediators of Inflammation

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Periodontal disease (PD) is a common infectious and inflammatory disease characterised by inflammation of tissues surrounding and supporting the teeth and destruction of the associated alveolar bone, eventually resulting in tooth loss. This disease is caused by periodontopathic bacteria in plaque biofilm and resultant innate and adaptive immune responses in periodontal tissues. Calprotectin (CLP) is a calcium-binding protein of the S-100 protein family and is found to be induced by activated granulocytes, monocytes, and epithelial cells. CLP has been shown to play an important role in numerous inflammatory diseases and disorders. Increasing evidence indicates that CLP is involved in the progression of PD, and its levels may be associated with disease severity and outcome of periodontal treatments. This review will summarise recent studies regarding the presence, regulation, and function of CLP in PD. The findings indicate that CLP may be an effective biomarker for diagnosis and treatment for the PD.

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Section: The Role Of Clp In Pdmentioning

confidence: 99%

Role of Calprotectin as a Biomarker in Periodontal Disease

Wei

Liu

Xiong

2019

Mediators of Inflammation

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“…Liu et al have recently reported that bacterial LPS inhibits osteoblastic differentiation and alkaline phosphatase (ALP) activity by suppressing the expressions of osteocalcin, Runx2, and ALP, and then downregulates bone matrix mineralization [10]. Moreover, LPS induces inflammatory cytokine levels, such as IL-1β, IL-6, IL-8, TNF-α, and S100A8/S100A9 from various cells in periodontal tissues [11][12][13]. In a recent study, high levels of calprotectin were detected in gingival crevicular fluid (GCF) from patients with periodontitis, and high levels of S100A8 and S100A9 were also detected in blood vessels in Pg-infected mice [14,15].…”

Section: Introductionmentioning

confidence: 99%

S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells

Takagi

Sakamoto

Kido

et al. 2020

BioMed Research International

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Objective. Calprotectin is a heterocomplex of S100A8 and S100A9 and is mainly secreted from neutrophils, monocytes, and chondrocytes in inflammatory condition. Calprotectin binds to RAGE and TLR4 and induces the expression of proinflammatory chemokines and cytokines in various cells. Periodontitis is a chronic inflammatory disease that leads to gingival inflammation and alveolar bone resorption. Calprotectin levels in gingival crevicular fluid of periodontitis patients are higher than healthy patients. In the present study, the effects of S100A8 and S100A9 on the expressions of proinflammatory cytokines and bone metabolism-related factors in mouse osteocyte-like cells (MLO-Y4-A2) were investigated. Design. MLO-Y4-A2 cells were treated with S100A8 and S100A9, and the expressions of RAGE, TLR4, RANKL, and several inflammatory cytokines were analyzed by PCR and Western blotting or ELISA methods. To investigate the intracellular signaling pathways, phosphorylation of MAPK and STAT3 was determined by Western blotting, and chemical specific inhibitors and siRNAs were used. Results. Expressions of IL-6 and RANKL were increased by treatment with S100A9 but not S100A8. However, both S100A8 and S100A9 did not change expression of IL-1β, IL-8, and TNF-α. Although RAGE and TLR4 expressions were not upregulated by S100A9 treatment, transfection of siRNA for RAGE and TLR4 significantly decreased IL-6 and RANKL expressions. In addition, S100A9 activated p38, ERK, and STAT3 signaling pathways, and inhibitors for these factors significantly decreased S100A9-induced IL-6 and RANKL expressions. Conclusions. These results indicated that S100A9 induces IL-6 and RANKL production via engagement with RAGE and TLR4 signalings in osteocytes and suggested that S100A9 may play important roles in the periodontal alveolar bone destruction.

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“…In another study, the neutrophils in diabetic mice produced more inflammatory cytokines, chemokines, superoxide, and an increase in neutrophil rolling and attachment on the vascular wall of gingival tissue was observed in vivo, 10 suggesting that the higher GCF level of calprotectin in DM‐P patients might also be due to the hyperinflammatory phenotype of neutrophil under high glucose environment. Besides, recent evidence has revealed that advanced glycation end products (AGEs) generated by chronic hyperglycemia up‐regulate the expression of S100A8 and S100A9 in a human gingival epithelial cell line, 32 which indicates gingival epithelial cells might be another resource for the elevated GCF level of calprotectin in DM‐P patients.…”

Section: Discussionmentioning

confidence: 99%

Calprotectin levels in gingival crevicular fluid and serum of patients with chronic periodontitis and type 2 diabetes mellitus before and after initial periodontal therapy

Gao

et al. 2020

J of Periodontal Research

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Background This study is aimed to compare the total amount of calprotectin in gingival crevicular fluid (GCF) and the concentration of calprotectin in serum among the patients with type 2 diabetes mellitus and chronic periodontitis (DM‐P), the patients with chronic periodontitis (CP) and the healthy controls, as well as the variation of these indicators before and three months after the initial periodontal therapy for the DM‐P patients. Methods 35 patients with DM‐P patients, 32 patients with CP patients, and 43 healthy controls were recruited. Calprotectin levels in serum and GCF, periodontal parameters, fasting blood glucose (FBG), and HbA1c were measured at baseline for all the groups and three months after the initial periodontal therapy for the DM‐P patients. Results At baseline, the calprotectin levels in GCF and serum were the highest in DM‐P, followed by CP, and the lowest in healthy controls. GCF calprotectin was significantly and positively correlated with serum calprotectin and probing depth (PD), while serum calprotectin had a significant positive correlation with GCF calprotectin and HbA1c. Periodontal parameters, HbA1c, and serum and GCF calprotectin became significantly reduced after the initial periodontal treatment. The reduction of serum calprotectin was consistent with that of HbA1c, while the decrease of GCF calprotectin was in agreement with that of PD, attachment loss (AL), and bleeding on probing (BOP). Conclusions The levels of calprotectin in serum and GCF in the DM‐P patients are significantly higher than those in CP patients and healthy controls, which significantly reduced 3 months after the initial periodontal therapy. Furthermore, it suggests diabetic patients might exhibit more pronounced inflammation periodontally and systemically.

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Advanced glycation end‐products and Porphyromonas gingivalis lipopolysaccharide increase calprotectin expression in human gingival epithelial cells

Cited by 25 publications

References 42 publications

Role of Calprotectin as a Biomarker in Periodontal Disease

Role of Calprotectin as a Biomarker in Periodontal Disease

S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells

Calprotectin levels in gingival crevicular fluid and serum of patients with chronic periodontitis and type 2 diabetes mellitus before and after initial periodontal therapy

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