Porphyromonas gingivalis GroEL Induces Osteoclastogenesis of Periodontal Ligament Cells and Enhances Alveolar Bone Resorption in Rats
Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue of HSP60, is significantly higher in periodontitis patients than in healthy control subjects, suggesting that P. gingivalis GroEL is a potenti...
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| Published in | PloS one Vol. 9; no. 7; p. e102450 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
24.07.2014
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1932-6203 1932-6203 |
| DOI | 10.1371/journal.pone.0102450 |
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| Abstract | Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue of HSP60, is significantly higher in periodontitis patients than in healthy control subjects, suggesting that P. gingivalis GroEL is a potential stimulator of periodontal disease. However, the specific role of GroEL in periodontal disease remains unclear. Here, we investigated the effect of P. gingivalis GroEL on human periodontal ligament (PDL) cells in vitro, as well as its effect on alveolar bone resorption in rats in vivo. First, we found that stimulation of PDL cells with recombinant GroEL increased the secretion of the bone resorption-associated cytokines interleukin (IL)-6 and IL-8, potentially via NF-κB activation. Furthermore, GroEL could effectively stimulate PDL cell migration, possibly through activation of integrin α1 and α2 mRNA expression as well as cytoskeletal reorganization. Additionally, GroEL may be involved in osteoclastogenesis via receptor activator of nuclear factor κ-B ligand (RANKL) activation and alkaline phosphatase (ALP) mRNA inhibition in PDL cells. Finally, we inoculated GroEL into rat gingiva, and the results of microcomputed tomography (micro-CT) and histomorphometric assays indicated that the administration of GroEL significantly increased inflammation and bone loss. In conclusion, P. gingivalis GroEL may act as a potent virulence factor, contributing to osteoclastogenesis of PDL cells and resulting in periodontal disease with alveolar bone resorption. |
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| AbstractList | Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue of HSP60, is significantly higher in periodontitis patients than in healthy control subjects, suggesting that P. gingivalis GroEL is a potential stimulator of periodontal disease. However, the specific role of GroEL in periodontal disease remains unclear. Here, we investigated the effect of P. gingivalis GroEL on human periodontal ligament (PDL) cells in vitro, as well as its effect on alveolar bone resorption in rats in vivo. First, we found that stimulation of PDL cells with recombinant GroEL increased the secretion of the bone resorption-associated cytokines interleukin (IL)-6 and IL-8, potentially via NF-κB activation. Furthermore, GroEL could effectively stimulate PDL cell migration, possibly through activation of integrin α1 and α2 mRNA expression as well as cytoskeletal reorganization. Additionally, GroEL may be involved in osteoclastogenesis via receptor activator of nuclear factor κ-B ligand (RANKL) activation and alkaline phosphatase (ALP) mRNA inhibition in PDL cells. Finally, we inoculated GroEL into rat gingiva, and the results of microcomputed tomography (micro-CT) and histomorphometric assays indicated that the administration of GroEL significantly increased inflammation and bone loss. In conclusion, P. gingivalis GroEL may act as a potent virulence factor, contributing to osteoclastogenesis of PDL cells and resulting in periodontal disease with alveolar bone resorption. Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue of HSP60, is significantly higher in periodontitis patients than in healthy control subjects, suggesting that P. gingivalis GroEL is a potential stimulator of periodontal disease. However, the specific role of GroEL in periodontal disease remains unclear. Here, we investigated the effect of P. gingivalis GroEL on human periodontal ligament (PDL) cells in vitro, as well as its effect on alveolar bone resorption in rats in vivo. First, we found that stimulation of PDL cells with recombinant GroEL increased the secretion of the bone resorption-associated cytokines interleukin (IL)-6 and IL-8, potentially via NF-κB activation. Furthermore, GroEL could effectively stimulate PDL cell migration, possibly through activation of integrin α1 and α2 mRNA expression as well as cytoskeletal reorganization. Additionally, GroEL may be involved in osteoclastogenesis via receptor activator of nuclear factor κ-B ligand (RANKL) activation and alkaline phosphatase (ALP) mRNA inhibition in PDL cells. Finally, we inoculated GroEL into rat gingiva, and the results of microcomputed tomography (micro-CT) and histomorphometric assays indicated that the administration of GroEL significantly increased inflammation and bone loss. In conclusion, P. gingivalis GroEL may act as a potent virulence factor, contributing to osteoclastogenesis of PDL cells and resulting in periodontal disease with alveolar bone resorption.Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue of HSP60, is significantly higher in periodontitis patients than in healthy control subjects, suggesting that P. gingivalis GroEL is a potential stimulator of periodontal disease. However, the specific role of GroEL in periodontal disease remains unclear. Here, we investigated the effect of P. gingivalis GroEL on human periodontal ligament (PDL) cells in vitro, as well as its effect on alveolar bone resorption in rats in vivo. First, we found that stimulation of PDL cells with recombinant GroEL increased the secretion of the bone resorption-associated cytokines interleukin (IL)-6 and IL-8, potentially via NF-κB activation. Furthermore, GroEL could effectively stimulate PDL cell migration, possibly through activation of integrin α1 and α2 mRNA expression as well as cytoskeletal reorganization. Additionally, GroEL may be involved in osteoclastogenesis via receptor activator of nuclear factor κ-B ligand (RANKL) activation and alkaline phosphatase (ALP) mRNA inhibition in PDL cells. Finally, we inoculated GroEL into rat gingiva, and the results of microcomputed tomography (micro-CT) and histomorphometric assays indicated that the administration of GroEL significantly increased inflammation and bone loss. In conclusion, P. gingivalis GroEL may act as a potent virulence factor, contributing to osteoclastogenesis of PDL cells and resulting in periodontal disease with alveolar bone resorption. Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue of HSP60, is significantly higher in periodontitis patients than in healthy control subjects, suggesting that P. gingivalis GroEL is a potential stimulator of periodontal disease. However, the specific role of GroEL in periodontal disease remains unclear. Here, we investigated the effect of P. gingivalis GroEL on human periodontal ligament (PDL) cells in vitro, as well as its effect on alveolar bone resorption in rats in vivo. First, we found that stimulation of PDL cells with recombinant GroEL increased the secretion of the bone resorption-associated cytokines interleukin (IL)-6 and IL-8, potentially via NF-[kappa]B activation. Furthermore, GroEL could effectively stimulate PDL cell migration, possibly through activation of integrin [alpha]1 and [alpha]2 mRNA expression as well as cytoskeletal reorganization. Additionally, GroEL may be involved in osteoclastogenesis via receptor activator of nuclear factor [kappa]-B ligand (RANKL) activation and alkaline phosphatase (ALP) mRNA inhibition in PDL cells. Finally, we inoculated GroEL into rat gingiva, and the results of microcomputed tomography (micro-CT) and histomorphometric assays indicated that the administration of GroEL significantly increased inflammation and bone loss. In conclusion, P. gingivalis GroEL may act as a potent virulence factor, contributing to osteoclastogenesis of PDL cells and resulting in periodontal disease with alveolar bone resorption. Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue of HSP60, is significantly higher in periodontitis patients than in healthy control subjects, suggesting that P. gingivalis GroEL is a potential stimulator of periodontal disease. However, the specific role of GroEL in periodontal disease remains unclear. Here, we investigated the effect of P. gingivalis GroEL on human periodontal ligament (PDL) cells in vitro , as well as its effect on alveolar bone resorption in rats in vivo . First, we found that stimulation of PDL cells with recombinant GroEL increased the secretion of the bone resorption-associated cytokines interleukin (IL)-6 and IL-8, potentially via NF-κB activation. Furthermore, GroEL could effectively stimulate PDL cell migration, possibly through activation of integrin α1 and α2 mRNA expression as well as cytoskeletal reorganization. Additionally, GroEL may be involved in osteoclastogenesis via receptor activator of nuclear factor κ-B ligand (RANKL) activation and alkaline phosphatase (ALP) mRNA inhibition in PDL cells. Finally, we inoculated GroEL into rat gingiva, and the results of microcomputed tomography (micro-CT) and histomorphometric assays indicated that the administration of GroEL significantly increased inflammation and bone loss. In conclusion, P. gingivalis GroEL may act as a potent virulence factor, contributing to osteoclastogenesis of PDL cells and resulting in periodontal disease with alveolar bone resorption. |
| Audience | Academic |
| Author | Lin, Feng-Yen Yang, Shue-Fen Tsao, Nai-Wen Tsai, Chien-Sung Hung, Shan-Ling Huang, Chun-Yao Chang, Nen-Chung Lin, Yi-Wen Hsiao, Fung-Ping Shih, Chun-Ming |
| AuthorAffiliation | 2 Cardiovascular Research Center, Taipei Medical University Hospital, Taipei, Taiwan 1 Division of Cardiology, Taipei Medical University Hospital, Taipei, Taiwan 4 Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan 3 Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan 7 Department of Dentistry, National Yang-Ming University, Taipei, Taiwan 6 Division of Cardiovascular Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan 8 Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan University of California, Merced, United States of America 5 Division of Cardiovascular Surgery, Taipei Medical University Hospital, Taipei, Taiwan |
| AuthorAffiliation_xml | – name: 4 Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan – name: 6 Division of Cardiovascular Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan – name: University of California, Merced, United States of America – name: 1 Division of Cardiology, Taipei Medical University Hospital, Taipei, Taiwan – name: 3 Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan – name: 8 Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan – name: 2 Cardiovascular Research Center, Taipei Medical University Hospital, Taipei, Taiwan – name: 5 Division of Cardiovascular Surgery, Taipei Medical University Hospital, Taipei, Taiwan – name: 7 Department of Dentistry, National Yang-Ming University, Taipei, Taiwan |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25058444$$D View this record in MEDLINE/PubMed |
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| Copyright | COPYRIGHT 2014 Public Library of Science 2014 Lin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2014 Lin et al 2014 Lin et al |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: FYL YWL SLH. Performed the experiments: FPH. Analyzed the data: FPH CYH CMS NWT NCC. Contributed reagents/materials/analysis tools: CYH CMS NWT SFY CST. Wrote the paper: FYL YWL. |
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| PublicationYear | 2014 |
| Publisher | Public Library of Science Public Library of Science (PLoS) |
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| Snippet | Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue... Porphyromonas gingivalis is a major periodontal pathogen that contains a variety of virulence factors. The antibody titer to P. gingivalis GroEL, a homologue... |
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| SubjectTerms | Alkaline phosphatase Alveolar bone Alveolar Bone Loss - genetics Alveolar Bone Loss - metabolism Alveolar Bone Loss - microbiology Alveolar Bone Loss - pathology Animals Bacterial Proteins - genetics Bacterial Proteins - metabolism Bacterial Proteins - pharmacology Biocompatibility Biology Biology and Life Sciences Biomedical materials Bone loss Bone resorption Cardiology Cell activation Cell migration Chaperonin 60 - genetics Chaperonin 60 - metabolism Chaperonin 60 - pharmacology Collagen Computed tomography Cytokines Cytoskeleton Deoxyribonucleic acid Disease DNA Fibroblasts Gene expression Gene Expression Regulation Gum disease Heart surgery Heat shock proteins Homology Hospitals Host-Pathogen Interactions Hsp60 protein Humans Integrin alpha1 - genetics Integrin alpha1 - metabolism Integrin alpha2 - genetics Integrin alpha2 - metabolism Integrins Interleukin 8 Interleukin-6 - biosynthesis Interleukin-6 - metabolism Interleukin-8 - biosynthesis Interleukin-8 - metabolism Internal medicine Ligaments Male Medicine Medicine and Health Sciences Motility NF-kappa B - genetics NF-kappa B - metabolism NF-κB protein Osteoclastogenesis Osteoclasts - drug effects Osteoclasts - metabolism Osteoclasts - pathology Periodontal disease Periodontal diseases Periodontal ligament Periodontal Ligament - microbiology Periodontal Ligament - pathology Periodontitis Periodontitis - genetics Periodontitis - metabolism Periodontitis - microbiology Periodontitis - pathology Porphyromonas gingivalis Porphyromonas gingivalis - genetics Porphyromonas gingivalis - metabolism Porphyromonas gingivalis - pathogenicity RANK Ligand - genetics RANK Ligand - metabolism Rats Rats, Sprague-Dawley Recombinant Proteins - genetics Recombinant Proteins - metabolism Recombinant Proteins - pharmacology Research and Analysis Methods Review boards RNA Stimulators TRANCE protein Virulence Virulence (Microbiology) Virulence factors |
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| Title | Porphyromonas gingivalis GroEL Induces Osteoclastogenesis of Periodontal Ligament Cells and Enhances Alveolar Bone Resorption in Rats |
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