• Journal of Periodontal and Implant Science
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• v.33 no.4
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• pp.555-562
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• 2003

The present study has been performed to evaluate Porphyromonas gingivalis (P.gingivalis) heat shock protein(HSP)60 as a candidate vaccine to inhibit multiple bacteria-induced alveolar bone loss. Rats were immunized with P.gingivalis HSP60 and experimental alveolar bone loss was induced by infection with multiple periodonto -pathogenic bacteria. Post-immune rat anti-P.gingivalis HSP IgG levels were significantly elevated and have demonstrated highly significant inverse relationship with the amount of alveolar bone loss induced by multiple bacteria. Results from PCR detection of subgingival bacterial plaque indicated that the vaccine successfully eradicated the multiple pathogenic species. We concluded that P.gingivalis HSP60 could potentially be developed as a vaccine to inhibit periodontal disease induced by multiple pathogenic bacteria.

• Korean Journal of Microbiology
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• v.53 no.4
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• pp.334-336
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• 2017

Porphyromonas gingivalis is a Gram-negative, obligately anaerobic, and nonmotile rod. P. gingivalis is a pathogen of periodontitis and endodontic infection as well as is associated with systemic diseases including atherosclerosis, preterm, and Alzheimer's diseases. P. gingivalis KCOM 2797 (= JS2) was isolated from a human periodontitis lesion. Here, we present the draft genome sequence of P. gingivalis KCOM 2797.

• Journal of Periodontal and Implant Science
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• v.33 no.3
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• pp.331-340
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• 2003

본 연구의 목적은 인간의 동맥경화증에서 Porphyromonas gingivalis (P. gingivalis)와 인체 열충격단백 60의 T-세포 및 교차성 B-세포 epitope를 규명하고 수립된 T-세포주의 T-세포 주요조직적합체 양상을 파악하려는 데 있다. P. gingivalis 열충격단백-반응성 T 세포주와 환자의 혈청을 이용하여 P. gingivalis 열충격단백60 분자를 구성하는 104개의 중복성 합성 펩타이드의 T-세포 epitope과 B-세포 epitope을 규명하였다. 인체 열충격단백60에 대한 B-세포 epitope도 같은 방법으로 파악하였다. P. gingivalis, P. gingivalis 열충격단백60 또는 인체 열충격단백60에 대한 IgG 항체는 모든 동맥경화증 환자에서 상승하였다. P. gingivalis 열충격단백60의 3, 15, 24, 33, 45, 53, 64, 84, 88, 99번 펩타이드가 주요한 T-세포 epitope였고 이것들은 T-세포 및 B-세포 공동 epitope이기도 했다. 또한 인체 열충격단백60 교차반응 B-세포 epitope은 15, 29, 53, 56, 69, 74번 펩타이드로 판명되었다. 대부분 환자의 주요조직적합체는 $HLA-DRB1^{\ast}1504$와 $HLA-DZB1^{\ast}0603$으로 나타났다. 결론적으로 P. gingivalis 열충격단백60은 제 2급 주요조직적합제-제한적으로 분해되고 전달되었으며 이 단백질이 공통적인 T-세포 및 B-세포 epitope를 가지면서 동시에 인체 열충격단백60과 교차성 B-세포 epitope을 가지면서 동맥경화증의 면역조절기능에 관여한다고 볼 수 있다.

• Journal of Periodontal and Implant Science
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• v.33 no.4
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• pp.543-553
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• 2003

Due to considerably high degree of sequence homology between bacterial and human heat shock proteins(hsp), it has been widely thought that this protein might be involved in autoimmune disease mechanisms in humans. To elucidate how stress proteins contribute in the immunopathogenesis of periodontitis, the present study was performed to evaluate the T cell immune responses specific to Porphyromonas gingivalis (P. gingivalis) heat shock protein (hsp)60 and T-cell epitope specificities for P. gingivalis hsp60 in periodontitis. Anti-P. gingivalis IgG antibody titers were elevated in all patients. We could establish P. gingivalis hsp-specific T cell ines from the peripheral blood of peridontitis, a mixture of $CD4^+$ and $CD8^+$ cells. Of 108 overlapping synthetic peptides spanning whole P. gingivalis hsp60 moleculc, ten peptides with cpitopes specifities for T-cell were showed. Interestingly, ten epitopes were also identified as T-cell epitopes in the present study as well as B-cell epitopes in peridontitis. Therefore, all the ten representative epitopes were designated as common T-and B-cell epitopes for peridontitis. It is critical in developing a peptide vaccine strategy for potential prevention of periodontitis. It was concluded that P. gingivalis hsp60 might be involved in the immunoregulatory process of periodontitis with heat shock protein specificities.

• International Journal of Oral Biology
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• v.43 no.4
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• pp.201-207
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• 2018

Porphyromonas gingivalis is among the major etiological pathogens of chronic periodontitis. The virulence mechanisms of P. gingivalis is yet to be identified as its activity is largely unknown in actual disease process. The purpose of this study is to identify antigens of P. gingivalis expressed only in patients with chronic periodontitis using a unique immunoscreening technique. Change Mediated Antigen Technology (CMAT), an antibody-based screening technique, was used to identify virulence-associated proteins of P. gingivalis that are expressed only during infection stage in patients having chronic periodontitis. Out of 13,000 recombinant clones screened, 22 tested positive for reproducible reactivity with rabbit hyperimmune anti-sera prepared against dental plaque samples acquired from periodontitis patients. The DNA sequences of these 18 genes were determined. CMAT-identified protein antigens of P. gingivalis included proteins involved in energy metabolism and biosynthesis, heme and iron binding, drug resistance, specific enzyme activities, and unknown functions. Further analysis of these genes could result in a novel insight into the virulence mechanisms of P. gingivalis.

• International Journal of Oral Biology
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• v.31 no.1
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• pp.21-26
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• 2006

Periodontopathogens including Porphyromonas gingivalis interact with host periodontal cells and the excessive subsequent host responses contribute a major part to the development of periodontal diseases. Cyclooxygenase(COX)-2-synthesized $PGE_2$ has detrimental activities in terms of periodontal pathogenesis. The present study investigated induction of COX-2 expression by P. gingivalis in human monocytic THP-1 cells. Live P. gingivalis increased expression of COX-2, but not that of COX-1, which was demonstrated at both mRNA and protein levels. Elevated levels of $PGE_2$ were released from P. gingivalis-infected THP-1 cells. Pharma-cological inhibition of p38 mitogen-activated protein kinase(MAPK) and extracellular signal-regulated kinase(ERK) substantially attenuated P. gingivalis-induced COX-2 mRNA expression. Indeed, activation of p38 MAPK and ERK was observed in P. gingivalis-infected THP-1 cells. Also, P. gingivalis induced activation of nuclear $factor-{\kappa}B\;(NF-{\kappa}B)$ which is an important transcription factor for COX-2. These results suggest that COX-2 expression is up regulated in P. gingivalis-infected monocytic cells, at least in part, via p38 MAPK, ERK, and $NF-{\kappa}B$.

• Journal of Periodontal and Implant Science
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• v.23 no.1
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• pp.1-15
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• 1993

P. gingivalis has been implicated as a strong pathogen in periodontal disease and known to have three serotypes of P. gingivalis. The purpose of this study is to investigate on the relationship between virulence, metabolic acids and genetic heterogeneity of P. gingivalis. P. gingivalis W50 standard strain and five strains of P. gingivalis serotype b Korean isolates were used in this study. For in vitro virulence test, lyophilized whole cell P. gingivalis were suspended, and sonicated with ultrasonic dismembranometer. Sonicated samples were applied to cultured cells derived from periodontal ligament, and cell activity was assayed with growth and survival assay. The metabolic acids were also extracted, and determined by High Performance Liquid Chromatography. Pst I-digested bacterial genomic DNA was electrophoresed, and densitometric analysis was performed to study the genetic heterogeneity. All of the P. gingivalis serotype b produced butyric acid. In cell activity study, butyric acid inhibited the cell activity irrespective of its concentration. Densitometric analysis showed restriction fragment length polymorphism. These results suggested that there existed heterogeneity of the metabolic acids and the virulence of P. gingivalis and such heterogeneity might be related to genetic heterogeneity.

• International Journal of Oral Biology
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• v.42 no.4
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• pp.149-153
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• 2017

Cyclooxygenase-2 (COX-2)-mediated prostaglandin $E_2$ ($PGE_2$) plays a key role in development and progression of inflammatory responses and Porphyromonas gingivalis is a common endodontic pathogen. In this study, we investigated induction of COX-2 and $PGE_2$ by P. gingivalis in human dental pulp cells (HDPCs). P. gingivalis increased expression of COX-2, but not that of COX-1. Increased levels of $PGE_2$ were released from P. gingivalis-infected HDPCs and this $PGE_2$ increase was blocked by celecoxib, a selective COX-2 inhibitor. P. gingivalis activated all three types of mitogen-activated protein kinases (MAPKs). P. gingivalis-induced activation of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) was demonstrated by the results of phosphorylation of $NF-{\kappa}B$ p65 and degradation of inhibitor of ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$). Pharmacological inhibition of each of the three types of MAPKs and $NF-{\kappa}B$ substantially attenuated P. gingivalis-induced $PGE_2$ production. These results suggest that P. gingivalis should promote endodontic inflammation by stimulating dental pulp cells to produce $PGE_2$.

• Journal of Periodontal and Implant Science
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• v.46 no.1
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• pp.2-9
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• 2016

Purpose: Porphyromonas gingivalis and Tannerella forsythia have been implicated as the major etiologic agents of periodontal disease. These two bacteria are frequently isolated together from the periodontal lesion, and it has been suggested that their interaction may increase each one's virulence potential. The purpose of this study was to identify proteins on the surface of these organisms that are involved in interbacterial binding. Methods: Biotin labeling of surface proteins of P. gingivalis and T. forsythia and liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis was performed to identify surface proteins involved in the coaggregating activity between P. gingivalis and T. forsythia. Results: It was found that three major T. forsythia proteins sized 161, 100, and 62 kDa were involved in binding to P. gingivalis, and P. gingivalis proteins sized 35, 32, and 26 kDa were involved in binding to T. forsythia cells. Conclusions: LC-MS/MS analysis identified one T. forsythia surface protein (TonB-linked outer membrane protein) involved in interbacterial binding to P. gingivalis. However, the nature of other T. forsythia and P. gingivalis surface proteins identified by biotin labeling could not be determined. Further analysis of these proteins will help elucidate the molecular mechanisms that mediate coaggregation between P. gingivalis and T. forsythia.

• Journal of Periodontal and Implant Science
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• v.33 no.2
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• pp.179-191
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• 2003

Since periodontal infections are suggested as risk factors for the development of cardiovascular diseases, the present study was performed to evaluate the T cell immune responses specific to Pophylomonas gingivalis(P. gingivalis) heat shock protein(hsp) 60 and T-cell and B-cell epitope specificities for P. gingivalis hsp60 in atherosclerosis. Anti-P, gingivalis IgG antibody titers were elevated in all patients. We could establish P. gingivalis hsp-specific T cell lines from the atheroma lesions, a mixture of $CD4^+$ and $CD8^+$ cells producing the cytokines characteristic of both Th1 and Th2 subsets. of 108 overlapping synthetic peptides spanning whole P. gingivalis hsp60 molecule, ten peptides with common epitopes specificities for both T-cell and B-cell were identified. it was concluded that P. gingivalis hsp60 might K involved in the immunoregulatory process of atherosclerotic diseases with epitope specificities.