The Periodontal Pathogen Aggregatibacter Actinomycetemcomitans Deteriorates Ventricular Remodeling After Myocardial Infarction in Mice
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- Hanatani Tomoya
- Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
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- Suzuki Jun-ichi
- Department of Advanced Clinical Science and Therapeutics, The University of Tokyo
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- Ogawa Masahito
- Department of Advanced Clinical Science and Therapeutics, The University of Tokyo
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- Aoyama Norio
- Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
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- Kobayashi Naho
- Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
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- Hirata Yasunobu
- Department of Advanced Clinical Science and Therapeutics, The University of Tokyo
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- Nagai Ryozo
- Department of Cardiovascular Medicine, The University of Tokyo
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- Izumi Yuichi
- Department of Periodontology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University
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- Isobe Mitsuaki
- Department of Cardiovascular Medicine, Tokyo Medical and Dental University
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抄録
Chronic inflammation plays a fundamental role in coronary heart disease (CHD). Periodontal disease is a common infectious disease and is a potential source of systemic inflammation. However, the effect of periodontal infection on CHD has not yet been proven. The purpose of this study was to determine the effect of periodontopathic bacteria on experimental myocardial infarction (MI). We implanted a chamber into the subcutaneous tissue of each male mouse. Aggregatibacter actinomycetemcomitans (A.a. n = 8), which is a major periodontal pathogen, or PBS (n = 6) was injected into the chamber. Then, MI was induced by permanent ligation of the left anterior descending coronary artery. To exclude the nonspecific effect of the pathogen, we injected A.a. into the mice without MI (n = 4). The plasma level of anti-A.a. antibody was statistically higher in A.a.-infected mice than in vehicle control mice. Seven days after the myocardial ischemia, the A.a.-positive MI hearts showed a larger infarct size and length than the A.a.-negative MI mice. The A.a.-positive MI hearts showed more MOMA-2 positive myocardial infiltrating cells compared to the A.a.-negative MI mice. The injection of A.a. into the mice without MI did not affect their hearts. We concluded that a periodontal pathogen infection might deteriorate ventricular remodeling after MI through inflammatory cell infiltration.
収録刊行物
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- International Heart Journal
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International Heart Journal 53 (4), 253-256, 2012
一般社団法人 インターナショナル・ハート・ジャーナル刊行会