Human dental stem cells suppress PMN activity after infection with the periodontopathogens Prevotella intermedia and Tannerella forsythia

Hieke, Cathleen; Kriebel, Katja; Engelmann, Robby; Müller‐Hilke, Brigitte; Lang, Hermann; Kreikemeyer, Bernd

doi:10.1038/srep39096

Cited by 22 publications

(22 citation statements)

References 59 publications

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“…However, this was only obtained from a single cell line. Although Ca9-22 has been employed in many periodontal studies (47)(48)(49), it is important to confirm what we found in this study in other gingival epithelial cells to clarify the physiological relevance of our findings.…”

Section: Discussionsupporting

confidence: 74%

EBV LMP1 in Gingival Epithelium Potentially Contributes to Human Chronic Periodontitis via Inducible IL8 Production

Watanabe

Nodomi

Koike

et al. 2019

In Vivo

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Background/Aim: Human chronic periodontitis is a major health problem. Although some oral bacteria have been reported to be putative pathogens, Epstein-Barr virus (EBV) is reported to be associated with the progression of periodontitis. However, the role of EBV in the aetiology of periodontitis is unknown. Therefore, we investigated periodontal pathogenesis of EBV to confirm whether EBVencoded latent membrane protein 1 (LMP1) induces Interleukin-8 (IL8) production in human gingival cells. Materials and Methods: Real-time polymerase chain reaction, luciferase assay, enzyme-linked immunosorbent assay (ELISA), and western blotting were performed for determining IL8 mRNA expression, nuclear factor kappa B (NF-ĸB) transcription, IL8 production, and the phosphorylation of NF-ĸB p65 and Inhibitor of kappa B alpha (IĸBα), respectively, in Ca9-22 human gingival epithelial cells. Two LMP1 mutants lacking C-terminal activating region (CATR) domains responsible for activating NF-ĸB were used. Results: Extremely high IL8 production was induced by LMP1 in time-and dose-dependent manner, where simultaneous phosphorylation of NF-κB p65 and IĸBα and transcription of NF-ĸB were observed. On the contrary, IL8 production and NF-ĸB transcription were drastically inhibited by dominant negative mutant of IĸBα. Moreover, the LMP1 mutants failed to induce IL8 production. Conclusion: Our findings suggest that due to CATR domains, LMP1 contributes to the progression of periodontitis via IL8 production attributable to NF-ĸB activation. Chronic periodontitis, a chronic inflammatory and infectious disease causing the destruction of the periodontium including the alveolar bone, is prevalent worldwide (1, 2). Mounting evidence has indicated that chronic periodontitis is a risk factor for pre-term birth, heart disease, diabetes, and atherosclerosis (1, 2). Over the past decade, neutrophil infiltration in the periodontium has been revealed to be the major aetiology for periodontitis (2). Some oral endogenous bacteria are believed to trigger periodontitis via host-parasite interactions (2, 3). However, periodontopathic bacteria, such as Porphyromonas gingivalis, are not always detected in periodontal lesions (4-6); therefore, the conventional theory based on bacterial aetiology alone cannot fully explain the aetiology of periodontitis. A positive association has been reported between chronic periodontitis and Epstein-Barr virus (EBV) infection (7-11). EBV, a member of the herpesvirus family, infects many adults. During primary EBV infection, the virus undergoes lytic replication in B-cells and epithelial cells of the upper aerodigestive tract, where it later establishes latency (12, 13). EBV can be reactivated and is commonly found in the saliva of infected people (9, 10, 14). Many reports have demonstrated that the amount of EBV DNA detected in 1793 This article is freely accessible online.

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Section: Discussionsupporting

confidence: 74%

EBV LMP1 in Gingival Epithelium Potentially Contributes to Human Chronic Periodontitis via Inducible IL8 Production

Watanabe

Nodomi

Koike

et al. 2019

In Vivo

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“…Thereafter, additional studies revealed that human dental follicle stem cells (hDFSCs) elicit a reduced pro-inflammatory response following bacterial infection, as compared to differentiated cells ( Biedermann et al, 2014 ). Furthermore, Kriebel et al (2013) and Biedermann et al (2014) showed that stem cell functions were influenced by oral bacteria in vitro , while Hieke et al (2016) found that infection with viable bacteria induced distinct reactions by stem cells that were different from reactions to a single administration of LPS ( Hieke et al, 2016 ). Thus, infected stem cells showed a reduced capacity for migration, though that finding is inconsistent with another study that demonstrated increased migration following stimulation with LPS ( Chatzivasileiou et al, 2013 ).…”

Section: Host–pathogen Interaction and Molecular Effects On Host Cellmentioning

confidence: 99%

Oral Biofilms from Symbiotic to Pathogenic Interactions and Associated Disease –Connection of Periodontitis and Rheumatic Arthritis by Peptidylarginine Deiminase

et al. 2018

Self Cite

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A wide range of bacterial species are harbored in the oral cavity, with the resulting complex network of interactions between the microbiome and host contributing to physiological as well as pathological conditions at both local and systemic levels. Bacterial communities inhabit the oral cavity as primary niches in a symbiotic manner and form dental biofilm in a stepwise process. However, excessive formation of biofilm in combination with a corresponding deregulated immune response leads to intra-oral diseases, such as dental caries, gingivitis, and periodontitis. Moreover, oral commensal bacteria, which are classified as so-called “pathobionts” according to a now widely accepted terminology, were recently shown to be present in extra-oral lesions with distinct bacterial species found to be involved in the onset of various pathophysiological conditions, including cancer, atherosclerosis, chronic infective endocarditis, and rheumatoid arthritis. The present review focuses on oral pathobionts as commensal and healthy members of oral biofilms that can turn into initiators of disease. We will shed light on the processes involved in dental biofilm formation and also provide an overview of the interactions of P. gingivalis, as one of the most prominent oral pathobionts, with host cells, including epithelial cells, phagocytes, and dental stem cells present in dental tissues. Notably, a previously unknown interaction of P. gingivalis bacteria with human stem cells that has impact on human immune response is discussed. In addition to this very specific interaction, the present review summarizes current knowledge regarding the immunomodulatory effect of P. gingivalis and other oral pathobionts, members of the oral microbiome, that pave the way for systemic and chronic diseases, thereby showing a link between periodontitis and rheumatoid arthritis.

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“…The effect of PDLSCs on neutrophils seems to be independent on cell-to-cell contact. Human DFSCs infected with periodontal pathogens P. intermedia or T. forsythia reduce neutrophil chemotaxis, phagocytic activity and NET formation [151]. Further investigations are needed to clarify the interactions between MSCs of dental origin and polymorphonuclear neutrophils as well as their underlying mechanisms.…”

Section: Polymorphonuclear Neutrophilsmentioning

confidence: 99%

Immunomodulatory Properties of Dental-Derived Mesenchymal Stem Cells

Andrukhov¹,

Behm²,

Blufstein³

et al. 2019

Periodontology and Dental Implantology

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Mesenchymal stem cells are considered as an attractive tool for tissue regeneration. Almost all dental tissues contain a population of MSC-like cells, which were extensively studied within the last few years. Besides their ability to differentiate into different cell types, dental MSCs also possess strong immunomodulatory properties. Dental MSCs modulate both innate and adaptive immune response and influence the activity of almost all components of the immune system. The interaction between dental MSCs and the immune system is reciprocal because immunomodulatory activity of MSCs is strongly regulated by cytokines produced by immune cells. MSCs isolated from inflamed tissues might exhibit impaired immunomodulatory capacity, suggesting a potential role of these cells in inflammatory diseases and particularly periodontitis. Recent studies suggest that immunomodulatory properties of MSCs can also play an important role in their tissue regenerative capacity. The therapeutic effects of MSCs, including their immunomodulatory capacity, are largely explained by their tropic activity, including production of immunomodulatory proteins and growth factors. Summarizing, dental MSCs play an important role in tissue homeostasis under healthy and diseased conditions.

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Human dental stem cells suppress PMN activity after infection with the periodontopathogens Prevotella intermedia and Tannerella forsythia

Cited by 22 publications

References 59 publications

EBV LMP1 in Gingival Epithelium Potentially Contributes to Human Chronic Periodontitis via Inducible IL8 Production

EBV LMP1 in Gingival Epithelium Potentially Contributes to Human Chronic Periodontitis via Inducible IL8 Production

Oral Biofilms from Symbiotic to Pathogenic Interactions and Associated Disease –Connection of Periodontitis and Rheumatic Arthritis by Peptidylarginine Deiminase

Immunomodulatory Properties of Dental-Derived Mesenchymal Stem Cells

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