Human periodontal ligament fibroblasts synthesize C‐reactive protein and Th‐related cytokines in response to interleukin (<scp>IL</scp>)‐6 trans‐signalling

Hernández-Caldera, A.; Vernal, Rolando; Paredes, Rodolfo; Veloso, Pablo; Astorga, Jessica; Hernández, Marcela

doi:10.1111/iej.12872

Cited by 14 publications

(9 citation statements)

References 27 publications

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“…Inflammation is a complex cascade of events that may lead to its resolution or, alternatively, to its stalling into a chronic condition that renders the management of the clinical condition hard to accomplish. The molecular events involved in this scenario are: an exaggerated production of IL-6 [33] and the consequent activation of the transcription factor STAT3 [34] that primes the production and release of several additional cytokines that sustain and maintain the inflammatory state. Among those cytokines, IL-17A is of paramount importance in the context of oral disease.…”

Section: Discussionmentioning

confidence: 99%

β-Caryophyllene Reduces the Inflammatory Phenotype of Periodontal Cells by Targeting CB2 Receptors

et al. 2020

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Human gingival fibroblasts (GF) and human oral mucosa epithelial cells (EC) with an inflammatory phenotype represent a valuable experimental paradigm to explore the curative activity of agents to be used in oral mucositis. The role of cannabinoid receptor 2 (CB2) has not yet been investigated in oral mucositis. The aim of this study was to evaluate the therapeutic potential of β-Caryophyllene (BCP), a CB2 agonist, in an in vitro model of oral mucositis. GF and EC were stimulated with LPS (2 µg/mL) alone or in combination with BCP; a group of LPS challenged GF and EC were treated with BCP and AM630, a CB2 antagonist. LPS increased the inflammatory cytokines TNF-α, IL-1β, IL-6 and IL-17A whereas it decreased the anti-inflammatory cytokine IL-13. The upstream signals were identified in an augmented expression of NF-κB and STAT-3 and in reduced mRNA levels of PPARγ and PGC-1α. BCP blunted the LPS-induced inflammatory phenotype and this effect was reverted by the CB2 antagonist AM630. These results suggest that CB2 receptors are an interesting target to develop innovative strategies for oral mucositis and point out that BCP exerts a marked curative effect in a preclinical model of oral mucositis which deserves to be confirmed in a clinical setting.

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Section: Discussionmentioning

confidence: 99%

β-Caryophyllene Reduces the Inflammatory Phenotype of Periodontal Cells by Targeting CB2 Receptors

et al. 2020

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“…In the current study, we found statistically higher CRP levels in GCF from individuals affected by both periodontitis and gingivitis, compared to healthy ones. Considering the lack of an evident association between periodontal disease and serum CRP levels found in our study, the aforementioned fact might be explained, to some extent, by a local production of CRP within periodontal tissues, which has been previously reported and demonstrated [19,40]. However, moderate to strong positive correlations between the concentrations of this protein in GCF and serum were also evidenced in all study groups, showing that CRP measurements in GCF may reflect its serum levels, as demonstrated in past works [18,25].…”

Section: Discussionmentioning

confidence: 49%

Assessment of Cardiovascular Risk in Women with Periodontal Diseases According to C-reactive Protein Levels

et al. 2021

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Cardiovascular diseases (CVD) are highly prevalent non-communicable diseases worldwide. Periodontitis may act as a non-traditional cardiovascular risk (CVR) factor, linked by a low-grade systemic inflammation mediated by C-reactive protein (CRP). Patients with periodontitis reported higher serum CRP levels; however, a CRP systemic and periodontal correlation in gingival crevicular fluid (GCF) and its CVR impact have been barely studied. We aimed to assess the association between periodontal diseases and CVR in a group of adult women, based on serum high-sensitivity CRP (hs-CRP) levels; and secondly, to determine the association between serum and GCF CRP levels. Gingival crevicular fluid and blood samples were obtained from women with periodontitis, gingivitis, and healthy controls. Serum and GCF CRP were determined by turbidimetric method and Luminex technology, respectively. Data were analyzed and adjusted by CVR factors. All women presented moderate CVR, without an evident association between serum hs-CRP levels and periodontal diseases. While serum hs-CRP concentrations did not significantly differ between groups, patients with gingivitis and periodontitis showed higher CRP levels in GCF, which positively correlated to CRP detection in serum.

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“…The pathological features of periapical periodontitis are inflammation of the apical area and destruction of bone tissue (Hernández et al, 2018, Kirkevang, Ørstavik, Bahrami, Wenzel, & Vaeth, 2017Wei, Liu, Xiong, Peng, 2018). This results in immune inflammatory responses, which involve a large number of inflammatory cells that are regulated by a variety of cytokines (Provenzano et al, 2016;Sasaki et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

JAK2‐STAT3 signaling pathway is involved in rat periapical lesions induced by Enterococcus faecalis

Wang

Jin

et al. 2019

Oral Diseases

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Objectives This study aimed to investigate the role of JAK2‐STAT3 (Janus kinase 2/signal transducer and activator of transcription 3) in periapical disease caused by Enterococcus faecalis, as well as the correlation between lipoteichoic acid (LTA) in E. faecalis and the activity of the JAK2‐STAT3 signaling pathway and osteoclast formation. Materials and Methods A rat model of periapical periodontitis induced by E. faecalis was established. Periapical bone resorption was confirmed by HE staining. The expression of JAK2, p‐JAK2, STAT3, and p‐STAT3 was assessed with immunohistochemical staining. Osteoclasts were observed through enzyme histochemical staining. LTA acted on mouse osteoclast precursor cells (RAW264.7 cells); a JAK2 inhibitor (AG490) was used to inhibit the JAK2‐STAT3 pathway in RAW264.7 cells. The expression of proteins in the JAK2‐STAT3 pathway and TRAP (tartrate resistant acid phosphatase) in RAW264.7 cells was also detected. Results Rat periapical periodontitis was successfully established and bone resorption peaked at day 21. The expression of critical components in the JAK2‐STAT3 pathway increased with the progression of inflammation. LTA promoted the differentiation of RAW264.7 cells into osteoclasts. NFATc1 was highly expressed and was inhibited by AG490. Conclusions JAK2‐STAT3 signaling pathway plays an important role in the process of periapical bone resorption and osteoclastogenesis.

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Human periodontal ligament fibroblasts synthesize C‐reactive protein and Th‐related cytokines in response to interleukin (IL)‐6 trans‐signalling

Abstract: IL-6 trans-signalling induced Th1 and Th17-related cytokines and represents an extra-hepatic mechanism for PCR synthesis in human periodontal ligament fibroblasts, contributing to explain the bone-destructive phenotype of apical lesions and eventually its systemic complications.

Cited by 14 publications

References 27 publications

β-Caryophyllene Reduces the Inflammatory Phenotype of Periodontal Cells by Targeting CB2 Receptors

β-Caryophyllene Reduces the Inflammatory Phenotype of Periodontal Cells by Targeting CB2 Receptors

Assessment of Cardiovascular Risk in Women with Periodontal Diseases According to C-reactive Protein Levels

JAK2‐STAT3 signaling pathway is involved in rat periapical lesions induced by Enterococcus faecalis

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