Antibody and T Cell Responses to Fusobacterium nucleatum and Treponema denticola in Health and Chronic Periodontitis

Shin, Jieun; Kho, Sang-A; Choi, Yun Sik; Kim, Yong C.; Rhyu, In‐Chul; Choi, Youngok

doi:10.1371/journal.pone.0053703

Cited by 14 publications

(15 citation statements)

References 49 publications

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“…Td92, a surface protein of T. denticola , induced the production of IFN‐γ but inhibited the secretion of IL‐4 by peripheral blood mononuclear cells from both healthy subjects and patients with chronic periodontitis. However, the patients presented a reduced IFN‐γ/IL‐4 cytokine balance, and the Td92‐induced IFN‐γ levels were negatively associated with periodontal destruction in these patients .…”

Section: Persistence Of Periodontal Pathogensmentioning

confidence: 91%

Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

Choi

2014

J of Periodontal Research

122

103

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Periodontitis is chronic inflammation of the periodontium caused by the host's inflammatory response to plaque biofilm, which destroys tooth-supporting soft and hard tissues. Periodontitis is a complex disease that involves interactions among three main features -microbial challenge, the host immune response, and environmental and genetic risk factors -in its pathogenesis. Although periodontitis has been regarded as the result of hyperimmune or hyperinflammatory responses to plaque bacteria, recent studies indicate that periodontal pathogens are rather poor activators and/or suppressors of the host immune response. This raises the question of how periodontal pathogens cause inflammation. To resolve this issue, in the present review we propose that bacterial invasion into gingival tissue is a key event in the initiation of periodontitis and that the persistence of these bacteria within host tissue results in chronic inflammation. In support of this hypothesis, we present the ways in which microbial, environmental and genetic risk factors contribute to bacterial invasion. It is hoped that the current model will instigate active discussion and new research to complete the puzzle of this complex disease process.

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Section: Persistence Of Periodontal Pathogensmentioning

confidence: 91%

Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

Choi

2014

J of Periodontal Research

122

103

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“…Periodontitis affects many people worldwide and is the main cause of tooth loss, whereas its pathogenesis is quite complicated. In general, periodontitis is an inflammatory disease, usually initiated by periodontal pathogens residing in the dental plaque, including Porphyromonas gingivalis (P. gingivilas) (Byrne et al, 2009), Aggregatibacter actinomycetemcomitans (A. actionomycetecomitans or Aa) (Fine et al, 2007), Tannerella forsythia (T. forsythia) (Tomita et al, 2013), Fusobacterium nucleatum (F. nucleatum), Treponema denticola (T. denticola) (Shin et al, 2013), and Actinomyces viscosus (A. viscosus) (Shimada et al, 2012). However, other risk factors, such as smoking (Kamma et al, 2004), dental calculus (Susin and Albandar, 2005), occlusal trauma (Nakatsu et al, 2014), mouth breathing (Seo et al, 2013), genetic factors (Laine et al, 2012), hormones (Antonoglou et al, 2015), and stress (Huang et al, 2011), can promote the progression of periodontitis.…”

Section: Introductionmentioning

confidence: 99%

Programmed cell death in periodontitis: recent advances and future perspectives

et al. 2016

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Periodontitis is a highly prevalent infectious disease, characterized by destruction of the periodontium, and is the main cause of tooth loss. Periodontitis is initiated by periodontal pathogens, while other risk factors including smoking, stress, and systemic diseases aggravate its progression. Periodontitis affects many people worldwide, but the molecular mechanisms by which pathogens and risk factors destroy the periodontium are unclear. Programmed cell death (PCD), different from necrosis, is an active cell death mediated by a cascade of gene expression events and can be mainly classified into apoptosis, autophagy, necroptosis, and pyroptosis. Although PCD is involved in many inflammatory diseases, its correlation with periodontitis is unclear. After reviewing the relevant published articles, we found that apoptosis has indeed been reported to play a role in periodontitis. However, the role of autophagy in periodontitis needs further verification. Additionally, implication of necroptosis or pyroptosis in periodontitis remains unknown. Therefore, we recommend future studies, which will unravel the pivotal role of PCD in periodontitis, allowing us to prevent, diagnose, and treat the disease, as well as predict its outcomes.

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“…For example, F. nucleatum FadA and the fimbriae of P. gingivalis play important roles in the attachment to and invasion of host cells [ 27 , 28 ]. Although the levels of antibodies specific to these adhesins in the phIgG were not determined, the presence of IgG specific to FadA or P. gingivalis fimbriae in the sera from both healthy individuals and patients with periodontitis has been reported [ 29 , 30 ]. The inhibition of the invasion of P. gingivalis by antibodies to beta 1 integrin, an epithelial cell receptor for the P. gingivalis fimbriae, has been demonstrated [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

N-acetylcysteine and the human serum components that inhibit bacterial invasion of gingival epithelial cells prevent experimental periodontitis in mice

Alam

Baek

Choi

et al. 2014

J Periodontal Implant Sci

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PurposeWe previously reported that human serum significantly reduces the invasion of various oral bacterial species into gingival epithelial cells in vitro. The aims of the present study were to characterize the serum component(s) responsible for the inhibition of bacterial invasion of epithelial cells and to examine their effect on periodontitis induced in mice.MethodsImmortalized human gingival epithelial (HOK-16B) cells were infected with various 5- (and 6-) carboxy-fluorescein diacetate succinimidyl ester-labeled oral bacteria, including Fusobacterium nucleatum, Provetella intermedia, Porphyromonas gingivalis, and Treponiema denticola, in the absence or presence of three major serum components (human serum albumin [HSA], pooled human IgG [phIgG] and α1-antitrypsin). Bacterial adhesion and invasion were determined by flow cytometry. The levels of intracellular reactive oxygen species (ROS) and activation of small GTPases were examined. Experimental periodontitis was induced by oral inoculation of P. gingivalis and T. denticola in Balb/c mice.ResultsHSA and phIgG, but not α1-antitrypsin, efficiently inhibited the invasion of various oral bacterial species into HOK-16B cells. HSA but not phIgG decreased the adhesion of F. nucleatum onto host cells and the levels of intracellular ROS in HOK-16B cells. N-acetylcysteine (NAC), a ROS scavenger, decreased both the levels of intracellular ROS and invasion of F. nucleatum into HOK-16B cells, confirming the role of ROS in bacterial invasion. Infection with F. nucleatum activated Rac1, a regulator of actin cytoskeleton dynamics. Not only HSA and NAC but also phIgG decreased the F. nucleatum-induced activation of Rac1. Furthermore, both HSA plus phIgG and NAC significantly reduced the alveolar bone loss in the experimental periodontitis induced by P. gingivalis and T. denticola in mice.ConclusionsNAC and the serum components HSA and phIgG, which inhibit bacterial invasion of oral epithelial cells in vitro, can successfully prevent experimental periodontitis.Graphical Abstract

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Antibody and T Cell Responses to Fusobacterium nucleatum and Treponema denticola in Health and Chronic Periodontitis

Cited by 14 publications

References 49 publications

Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

Bacterial invasion and persistence: critical events in the pathogenesis of periodontitis?

Programmed cell death in periodontitis: recent advances and future perspectives

N-acetylcysteine and the human serum components that inhibit bacterial invasion of gingival epithelial cells prevent experimental periodontitis in mice

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