JAK/STAT Pathway Modulates on <i>Porphyromonas gingivalis </i>Lipopolysaccharide- and Nicotine-Induced Inflammation in Osteoblasts

Han, Yang-keum; Lee, In Su; Lee, Sang‐im

doi:10.17135/jdhs.2017.17.1.81

Cited by 6 publications

(5 citation statements)

References 26 publications

(24 reference statements)

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“…Studies suggest that LPS and nicotine synergistically induce the production of cyclooxgenase-2 (COX-2) and prostaglandin E2 (PGE2) and increase JAK/STAT protein expression. Treatment with a JAK inhibitor blocks the production of COX-2 and PGE2 and the expression of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6 in LPS- and nicotine-stimulated osteoblasts 71,72 . PGE2 is associated with bone loss in periodontal disease, inducing MMPs and osteoclast absorption.…”

Section: Resultsmentioning

confidence: 99%

Effect of tobacco on periodontal disease and oral cancer

Zhang¹,

He²,

He³

et al. 2019

Tob. Induc. Dis.

111

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INTRODUCTION Periodontal disease and oral cancer are common health hazards. Epidemiological investigations show that smoking, periodontal disease and oral cancer are closely related. Tobacco is one of the major risk factors for periodontitis and oral cancer. METHODS A systematic literature review was performed. To identify relevant studies, the following online databases were searched using specific keywords: PubMed, Web of Science and CNKI. RESULTS Tobacco not only possesses an addictive effect, but it aggravates periodontal disease by promoting the invasion of pathogenic bacteria, inhibiting autoimmune defense, aggravating the inflammatory reaction, and aggravating the loss of alveolar bone. According to current evidence, tobacco significantly aggravates the development and progression of periodontal disease and oral cancer, and periodontal disease may be related to the prevalence of oral cancer. CONCLUSIONS Clinicians should strongly recommend that smokers undertake a strategy to stop smoking to avoid the exacerbation of nicotine-related periodontal disease and to reduce the incidence of oral cancer.

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Section: Resultsmentioning

confidence: 99%

Effect of tobacco on periodontal disease and oral cancer

Zhang¹,

He²,

He³

et al. 2019

Tob. Induc. Dis.

111

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“…The oral epithelium is the first tissue exposed to nicotine following tobacco smoking. Several pathways have been implicated in the deleterious effect of nicotine on periodontal cells homeostasis, including increasing autophagy and apoptosis in periodontal ligament cells via nicotinic acetylcholine receptor α7 and β4 subunits [ 15 , 16 ], modifying the migration of human gingival epithelial cells through the activation of the MAPK ERK1/2 and p38 signaling pathways [ 17 ], inducing the production of cyclooxygenase-2 and prostaglandin E2 in osteoblasts via the JAK/STAT pathway [ 18 ]. Until now, the effect of nicotine on the oral epithelium remains conflicting [ 19 , 20 ], with some findings reporting no influence on inflammatory factor production [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

Holl

Wang

et al. 2021

IJERPH

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Smoking is a well-recognized risk factor for oral mucosal and periodontal diseases. Nicotine is an important component of cigarette smoke. This study aims to investigate the impact of nicotine on the viability and inflammatory mediator production of an oral epithelial cell line in the presence of various inflammatory stimuli. Oral epithelial HSC-2 cells were challenged with nicotine (10−8–10−2 M) for 24 h in the presence or absence of Porphyromonas gingivalis lipopolysaccharide (LPS, 1 µg/mL) or tumor necrosis factor (TNF)-α (10−7 M) for 24 h. The cell proliferation/viability was determined by MTT assay. Gene expression of interleukin (IL)-8, intercellular adhesion molecule (ICAM)-1, and β-defensin was assayed by qPCR. The production of IL-8 protein and cell surface expression of ICAM-1 was assessed by ELISA and flow cytometry, respectively. Proliferation/viability of HSC-2 cells was unaffected by nicotine at concentrations up to 10−3 M and inhibited at 10−2 M. Nicotine had no significant effect on the basal expression of IL-8, ICAM-1, and β-defensin. At the same time, it significantly diminished P. gingivalis LPS or the TNF-α-induced expression levels of these factors. Within the limitations of this study, the first evidence was provided in vitro that nicotine probably exerts a suppressive effect on the production of inflammatory mediators and antimicrobial peptides in human oral epithelial cells.

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“…The expression of janus kinase (JAK)/signal transducer and activator of transcription (STAT) is modulated by P. gingivalis, objectified by the production of prostaglandin E2 and cyclooxgenase-2, and elevated the protein expression of JAK/STAT induced by lipopolysaccharide and nicotine. The addition of a JAK inhibitor blocked cyclooxgenase-2 and prostaglandin E2 production, but also the expression of TNF-α, IL-6, and IL-1β in osteoblasts stimulated with lipopolysaccharide and nicotine [83]. Tofacitinib was shown to ameliorate periodontal inflammation along with a decrease of IL-6, TNF-α, anti-cyclic citrullinated peptide immunoglobulin G and MMP-3 [84].…”

Section: Dmardsmentioning

confidence: 97%

The Effect of Acknowledged and Novel Anti-Rheumatic Therapies on Periodontal Tissues—A Narrative Review

et al. 2021

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Rheumatoid arthritis (RA) and periodontal disease (PD) are chronic complex inflammatory diseases with several common susceptibility factors, especially genetic and environmental risk factors. Although both disorders involve a perturbation of the immune–inflammatory response at multiple levels, one major difference between the two is the different locations in which they develop. RA is triggered by an exaggerated autoimmune response that targets joints, while periodontal disease occurs as a consequence of the subgingival periodontopathogenic microbiota. Current treatment models in both pathologies involve the stratification of patients to allow therapeutic individualization according to disease stage, complexity, progression, lifestyle, risk factors, and additional systemic diseases. Therapeutic guidelines for RA comprise of five main classes of drugs: non-steroidal anti-inflammatory drugs (NSAIDs), analgesics, glucocorticoids, and disease-modifying anti-rheumatic drugs (DMARDs): biologic and non-biologic. Although various treatment options are available, a definitive treatment remains elusive, therefore research is ongoing in this area. Several alternatives are currently being tested, such as matrix metalloproteinases (MMP) inhibitors, toll-like receptors (TLR) blockers, pro-resolution mediators, anti-hypoxia inducing factors, stem cell therapy, NLRP3 inhibitors and even natural derived compounds. Although the link between PD and rheumatoid arthritis has been investigated by multiple microbiology and immunology studies, the precise influence and causality is still debated in the literature. Furthermore, the immunomodulatory effect of anti-rheumatic drugs on the periodontium is still largely unknown. In this narrative review, we explore the mechanisms of interaction and the potential influence that anti-rheumatoid medication, including novel treatment options, has on periodontal tissues and whether periodontal health status and treatment can improve the prognosis of an RA patient.

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JAK/STAT Pathway Modulates on Porphyromonas gingivalis Lipopolysaccharide- and Nicotine-Induced Inflammation in Osteoblasts

Cited by 6 publications

References 26 publications

Effect of tobacco on periodontal disease and oral cancer

Effect of tobacco on periodontal disease and oral cancer

Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

The Effect of Acknowledged and Novel Anti-Rheumatic Therapies on Periodontal Tissues—A Narrative Review

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