Treponema denticola,Porphyromonas gingivalis,and Tannerella forsythia induce cell death and release of endogenous danger signals |
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| Affiliation: | 1. Department of Oral Microbiology and Immunology, School of Dentistry, Seoul National University, South Korea;2. Dental Research Institute, School of Dentistry, Seoul National University, South Korea;1. Department of Periodontology, School of Dental Medicine, University of Bern, Freiburgstrasse 7, CH-3010 Bern, Switzerland;2. Department of Periodontology, Faculty of Odontology, Malmö University, Malmö, Sweden;3. Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University in Krakow, Gronostajowa Krakow, Poland;4. Department of Conservative Dentistry and Periodontology, Poznan University of Medical Sciences, Poznan, Poland;1. Department of Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI, United States;2. Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, MI, United States;1. School of Veterinary Medicine, Universidade Estadual Paulista, Araçatuba, Brazil;2. Dental School, Universidade Estadual Paulista, Araçatuba, Brazil;3. School of Engineering, Universidade Estadual Paulista, Ilha Solteira, Brazil;4. School of Veterinary Medicine, University of Glasgow, Glasgow, UK;5. Dental School, University of Glasgow, Glasgow, UK;1. State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, 3rd Section S Renmin Road, 14#, Chengdu, PR China;2. Department of Prosthodontics, West China Hospital of Stomatology, Sichuan University, PR China;3. Department of Periodontology, West China Hospital of Stomatology, Sichuan University, PR China;4. Department of Implantology, West China Hospital of Stomatology, Sichuan University, PR China;1. Dept. of Oral Biology, University at Buffalo, Buffalo, NY, United States;2. Oral & Maxillofacial Pathology, The University of Sheffield, Sheffield, United Kingdom |
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| Abstract: | ObjectiveThe aim of this study was to analyze whether periodontopathogens induced inflammatory cell death and the release of diverse endogenous danger molecules in THP-1-derived macrophages.MethodsThe macrophages were treated with Treponema denticola, Porphyromonas gingivalis, and Tannerella forsythia. Activation of caspase-1 and caspase-4 was detected by Western blotting. Cell death of bacteria-stimulated macrophages was examined using a lactate dehydrogenase (LDH) assay and propidium iodide (PI)/annexin V (AV) staining. Levels of endogenous danger signals, including adenosine triphosphate (ATP), uric acid, heat shock protein 60 (HSP60), high-mobility group box protein 1 (HMGB1), and fibronectin in the culture supernatants were determined using an ATP bioluminescence assay kit, a uric acid assay kit, and Western blotting, respectively.ResultsT. denticola, P. gingivalis, and T. forsythia induced activation of caspase-1 and caspase-4. The LDH assay and PI/AV staining showed that all three pathogens induced pyroptotic cell death. All three bacteria induced release of ATP, which is an important ligand for inflammasome activation; the increase in ATP ultimately leads to caspase-1 activation. T. denticola induced release of HSP60 and fibronectin, while T. forsythia induced release of HMGB1 in addition to HSP60 and fibronectin. None of the endogenous molecules except for fibronectin were detected in P. gingivalis-infected cells, possibly due to degradation of these factors by the proteolytic activity of the bacteria. Interestingly, P. gingivalis induced uric acid release.ConclusionInflammatory cell death and endogenous danger molecules released from cells infected with periodontopathogens may play critical roles in the pathogenesis and progression of periodontitis by augmenting immune and inflammatory responses. |
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| Keywords: | Periodontopathogens Macrophages Inflammatory caspases Cell death Danger signals |
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