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Effect of Porphyromonas gingivalis Infection on PGC-1α in Skeletal Muscle After Endurance Training In Vivo.

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Τίτλος: Effect of Porphyromonas gingivalis Infection on PGC-1α in Skeletal Muscle After Endurance Training In Vivo.
Συγγραφείς: Hayashi K; Department of Masticatory Function and Health Science, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.; Division of Sports Dentistry, Sports Science Organization, Institute of Science Tokyo, Tokyo, Japan., Takeuchi Y; Department of Lifetime Oral Health Care Science, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan., Kobayashi H; Department of Periodontology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan., Tanabe G; Department of Sports Dentistry, Meikai University School of Dentistry, Sakado, Japan., Churei H; Department of Masticatory Function and Health Science, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.; Division of Sports Dentistry, Sports Science Organization, Institute of Science Tokyo, Tokyo, Japan., Ueno T; Department of Sports Dentistry, Meikai University School of Dentistry, Sakado, Japan., Fueki K; Department of Masticatory Function and Health Science, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Πηγή: Clinical and experimental dental research [Clin Exp Dent Res] 2026 Aug; Vol. 12 (4), pp. e70415.
Τύπος έκδοσης: Journal Article; Research Support, Non-U.S. Gov't
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Wiley Country of Publication: United States NLM ID: 101692332 Publication Model: Print Cited Medium: Internet ISSN: 2057-4347 (Electronic) Linking ISSN: 20574347 NLM ISO Abbreviation: Clin Exp Dent Res Subsets: MEDLINE
Imprint Name(s): Original Publication: Hoboken : Wiley, [2015]-
Ιατρικοί όροι (MeSH): Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha*/metabolism , Porphyromonas gingivalis*/immunology , Muscle, Skeletal*/metabolism , Muscle, Skeletal*/microbiology , Bacteroidaceae Infections*/metabolism , Bacteroidaceae Infections*/physiopathology , Bacteroidaceae Infections*/microbiology , Physical Conditioning, Animal* , Endurance Training*, Tumor Necrosis Factor-alpha/metabolism ; Immunoglobulin G/blood ; Antibodies, Bacterial/blood ; Animals ; Rats, Wistar ; Rats ; Male ; Physical Endurance
Περίληψη: Objectives: It is well known that Porphyromonas gingivalis, a major pathogen in periodontitis, causes systemic diseases. This study investigated the expression of PGC-1α (the most important factor in muscle mitochondria synthesis) following endurance training to clarify the relationship between P. gingivalis infection and muscle endurance capacity.
Materials and Methods: Twenty 8-week-old Wistar rats were randomly divided into two groups. One group was intraperitoneally administered sonicated P. gingivalis (P. g-group), and the other group was administered saline (Control-group). Three weeks after administration, gastrocnemius muscles and blood from both groups were collected 24 h after treadmill exercise. The expressions of PGC-1α and TNF-α in gastrocnemius muscle were measured, along with serum antibody titers for IgG, in response to P. gingivalis.
Results: Serum IgG antibody titers and TNF-α expression in skeletal muscle were significantly higher in the P. g-group than in the Control-group. PGC-1α expression was significantly lower in the P. g-group than in the Control-group. A correlation was observed between PGC-1α and TNF-α expression.
Conclusion: Our result suggests that the increase in endurance following training may be suppressed by P. gingivalis infection.
(© 2026 The Author(s). Clinical and Experimental Dental Research published by John Wiley & Sons Ltd.)
References: Baeza, M., A. Morales, C. Cisterna, et al. 2020. “Effect of Periodontal Treatment in Patients With Periodontitis and Diabetes: Systematic Review and Meta‐Analysis.” Journal of Applied Oral Science 28: e20190248. https://doi.org/10.1590/1678-7757-2019-0248.
Burns, E., G. Bachrach, L. Shapira, and G. Nussbaum. 2006. “Cutting Edge: TLR2 Is Required for the Innate Response to Porphyromonas gingivalis: Activation Leads to Bacterial Persistence and TLR2 Deficiency Attenuates Induced Alveolar Bone Resorption.” Journal of Immunology 177, no. 12: 8296–8300. https://doi.org/10.4049/jimmunol.177.12.8296.
Cardoso, E. M., C. Reis, and M. C. Manzanares‐Céspedes. 2018. “Chronic Periodontitis, Inflammatory Cytokines, and Interrelationship With Other Chronic Diseases.” Postgraduate Medicine 130, no. 1: 98–104. https://doi.org/10.1080/00325481.2018.1396876.
Carrouel, F., S. Viennot, J. Santamaria, P. Veber, and D. Bourgeois. 2016. “Quantitative Molecular Detection of 19 Major Pathogens in the Interdental Biofilm of Periodontally Healthy Young Adults.” Frontiers in Microbiology 7: 840. https://doi.org/10.3389/fmicb.2016.00840.
Chandel, N. S. 2021. “Mitochondria.” Cold Spring Harbor Perspectives in Biology 13, no. 3: a040543. https://doi.org/10.1101/cshperspect.a040543.
Cheng, Z., T. Do, K. Mankia, et al. 2021. “Dysbiosis in the Oral Microbiomes of Anti‐CCP Positive Individuals at Risk of Developing Rheumatoid Arthritis.” Annals of the Rheumatic Diseases 80, no. 2: 162–168. https://doi.org/10.1136/annrheumdis-2020-216972.
Dorn, B. R., L. J. Harris, C. T. Wujick, F. J. Vertucci, and A. Progulske‐Fox. 2002. “Invasion of Vascular Cells In Vitro by Porphyromonas endodontalis.” International Endodontic Journal 35, no. 4: 366–371. https://doi.org/10.1046/j.0143-2885.2001.00489.x.
Farenia, R., R. Lesmana, K. Uchida, T. Iwasaki, N. Koibuchi, and N. Shimokawa. 2019. “Changes in Biomarker Levels and Myofiber Constitution in Rat Soleus Muscle at Different Exercise Intensities.” Molecular and Cellular Biochemistry 458, no. 1–2: 79–87. https://doi.org/10.1007/s11010-019-03532-9.
Grenier, D., and S. Tanabe. 2010. “Porphyromonas gingivalis Gingipains Trigger a Proinflammatory Response in Human Monocyte‐Derived Macrophages Through the p38α Mitogen‐Activated Protein Kinase Signal Transduction Pathway.” Toxins 2, no. 3: 341–352. https://doi.org/10.3390/toxins2030341.
Hajishengallis, G., R. P. Darveau, and M. A. Curtis. 2012. “The Keystone‐Pathogen Hypothesis.” Nature Reviews Microbiology 10, no. 10: 717–725. https://doi.org/10.1038/nrmicro2873.
Hajishengallis, G., M. Wang, and S. Liang. 2009. “Induction of Distinct TLR2‐Mediated Proinflammatory and Proadhesive Signaling Pathways in Response to Porphyromonas gingivalis Fimbriae.” Journal of Immunology 182, no. 11: 6690–6696. https://doi.org/10.4049/jimmunol.0900524.
Hayashi, K., Y. Takeuchi, S. Shimizu, et al. 2022. “Continuous Oral Administration of Sonicated P. gingivalis Delays Rat Skeletal Muscle Healing Post‐Treadmill Training.” International Journal of Environmental Research and Public Health 19, no. 20: 13046. https://doi.org/10.3390/ijerph192013046.
Holt, S. C., and J. L. Ebersole. 2005. “Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia: The ‘Red Complex’, a Prototype Polybacterial Pathogenic Consortium in Periodontitis.” Periodontology, 2000 38: 72–122. https://doi.org/10.1111/j.1600-0757.2005.00113.x.
Kodama, S. 2009. “Cardiorespiratory Fitness as a Quantitative Predictor of All‐Cause Mortality and Cardiovascular Events in Healthy Men and Women: A Meta‐Analysis.” Journal of the American Medical Association 301, no. 19: 2024–2035. https://doi.org/10.1001/jama.2009.681.
Kojima, T., K. Yano, and I. Ishikawa. 1997. “Relationship Between Serum Antibody Levels and Subgingival Colonization of Porphyromonas gingivalis in Patients With Various Types of Periodontitis.” Journal of Periodontology 68, no. 7: 618–625. https://doi.org/10.1902/jop.1997.68.7.618.
Lesmana, R., T. Iwasaki, Y. Iizuka, I. Amano, N. Shimokawa, and N. Koibuchi. 2016. “The Change in Thyroid Hormone Signaling by Altered Training Intensity in Male Rat Skeletal Muscle.” Endocrine Journal 63, no. 8: 727–738. https://doi.org/10.1507/endocrj.EJ16-0126.
McGee, S. L., and M. Hargreaves. 2020. “Exercise Adaptations: Molecular Mechanisms and Potential Targets for Therapeutic Benefit.” Nature Reviews Endocrinology 16, no. 9: 495–505. https://doi.org/10.1038/s41574-020-0377-1.
Naderi, S., and A. T. Merchant. 2020. “The Association Between Periodontitis and Cardiovascular Disease: An Update.” Current Atherosclerosis Reports 22, no. 10: 52. https://doi.org/10.1007/s11883-020-00878-0.
Naruishi, K., and T. Nagata. 2018. “Biological Effects of Interleukin‐6 on Gingival Fibroblasts: Cytokine Regulation in Periodontitis.” Journal of Cellular Physiology 233, no. 9: 6393–6400. https://doi.org/10.1002/jcp.26521.
Ohtsu, A., Y. Takeuchi, S. Katagiri, et al. 2019. “Influence of Porphyromonas gingivalis in Gut Microbiota of Streptozotocin‐Induced Diabetic Mice.” Oral Diseases 25, no. 3: 868–880. https://doi.org/10.1111/odi.13044.
Olesen, J., K. Kiilerich, and H. Pilegaard. 2010. “PGC‐1α‐Mediated Adaptations in Skeletal Muscle.” Pflügers Archiv ‐ European Journal of Physiology 460, no. 1: 153–162. https://doi.org/10.1007/s00424-010-0834-0.
Olsen, I., and Ö. Yilmaz. 2016. “Modulation of Inflammasome Activity by Porphyromonas gingivalis in Periodontitis and Associated Systemic Diseases.” Journal of Oral Microbiology 8: 30385. https://doi.org/10.3402/jom.v8.30385.
Palomer, X., D. Álvarez‐Guardia, R. Rodríguez‐Calvo, et al. 2009. “TNF‐α Reduces PGC‐1α Expression Through NF‐κB and p38 MAPK Leading to Increased Glucose Oxidation in a Human Cardiac Cell Model.” Cardiovascular Research 81, no. 4: 703–712. https://doi.org/10.1093/cvr/cvn327.
Preshaw, P. M., A. L. Alba, D. Herrera, et al. 2012. “Periodontitis and Diabetes: A Two‐Way Relationship.” Diabetologia 55, no. 1: 21–31. https://doi.org/10.1007/s00125-011-2342-y.
Sanz, M., A. Marco Del Castillo, S. Jepsen, et al. 2020. “Periodontitis and Cardiovascular Diseases: Consensus Report.” Journal of Clinical Periodontology 47, no. 3: 268–288. https://doi.org/10.1111/jcpe.13189.
Socransky, S. S., A. D. Haffajee, M. A. Cugini, C. Smith, and R. L. Kent, Jr. 1998. “Microbial Complexes in Subgingival Plaque.” Journal of Clinical Periodontology 25, no. 2: 134–144. https://doi.org/10.1111/j.1600-051x.1998.tb02419.x.
Teshome, A., and A. Yitayeh. 2016. “Relationship Between Periodontal Disease and Preterm Low Birth Weight: Systematic Review.” Pan African Medical Journal 24: 215. https://doi.org/10.11604/pamj.2016.24.215.8727.
Udagawa, S., S. Katagiri, S. Maekawa, et al. 2018. “Effect of Porphyromonas gingivalis Infection in the Placenta and Umbilical Cord in Pregnant Mice With Low Birth Weight.” Acta Odontologica Scandinavica 76, no. 6: 433–441. https://doi.org/10.1080/00016357.2018.1426876.
Wang, D., G. Koshy, T. Nagasawa, et al. 2006. “Antibody Response After Single‐Visit Full‐Mouth Ultrasonic Debridement Versus Quadrant‐Wise Therapy.” Journal of Clinical Periodontology 33, no. 9: 632–638. https://doi.org/10.1111/j.1600-051X.2006.00963.x.
Watanabe, K., S. Katagiri, H. Takahashi, et al. 2021. “Porphyromonas gingivalis Impairs Glucose Uptake in Skeletal Muscle Associated With Altering Gut Microbiota.” FASEB Journal 35, no. 2: e21171. https://doi.org/10.1096/fj.202001158R.
Zhou, Q., T. Desta, M. Fenton, D. T. Graves, and S. Amar. 2005. “Cytokine Profiling of Macrophages Exposed to Porphyromonas gingivalis, Its Lipopolysaccharide, or Its FimA Protein.” Infection and Immunity 73, no. 2: 935–943. https://doi.org/10.1128/IAI.73.2.935-943.2005.
Grant Information: JP20K18822 JSPS KAKENHI
Contributed Indexing: Keywords: P. gingivalis; PGC‐1α; endurance training; skeletal muscle
Substance Nomenclature: 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
0 (Tumor Necrosis Factor-alpha)
0 (Ppargc1a protein, rat)
0 (Immunoglobulin G)
0 (Antibodies, Bacterial)
Entry Date(s): Date Created: 20260716 Date Completed: 20260716 Latest Revision: 20260726
Update Code: 20260726
PubMed Central ID: PMC13375082
DOI: 10.1002/cre2.70415
PMID: 42462077
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:2057-4347
DOI:10.1002/cre2.70415