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Porphyromonas gingivalis promotes murine abdominal aortic aneurysms via matrix metalloproteinase‐2 induction

Identifieur interne : 003A71 ( Istex/Corpus ); précédent : 003A70; suivant : 003A72

Porphyromonas gingivalis promotes murine abdominal aortic aneurysms via matrix metalloproteinase‐2 induction

Auteurs : N. Aoyama ; J. Suzuki ; D. Wang ; M. Ogawa ; N. Kobayashi ; T. Hanatani ; Y. Takeuchi ; Y. Izumi ; M. Isobe

Source :

RBID : ISTEX:76E5742732168605CD97F2A0485B44A88BB30C16

English descriptors

Abstract

Aoyama N, Suzuki J, Wang D, Ogawa M, Kobayashi N, Hanatani T, Takeuchi Y, Izumi Y, Isobe M. Porphyromonas gingivalis promotes murine abdominal aortic aneurysms via matrix metalloproteinase‐2 induction. J Periodont Res 2011; 46: 176–183. © 2010 John Wiley & Sons A/S

Url:
DOI: 10.1111/j.1600-0765.2010.01326.x

Links to Exploration step

ISTEX:76E5742732168605CD97F2A0485B44A88BB30C16

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<p>
<hi rend="italic">Aoyama N, Suzuki J, Wang D, Ogawa M, Kobayashi N, Hanatani T, Takeuchi Y, Izumi Y, Isobe M.</hi>
Porphyromonas gingivalis
<hi rend="italic">promotes murine abdominal aortic aneurysms via matrix metalloproteinase‐2 induction. J Periodont Res 2011; 46: 176–183. © 2010 John Wiley & Sons A/S</hi>
</p>
<p>
<hi rend="bold">Background and Objective: </hi>
Abdominal aortic aneurysm (AAA) is a common and lethal disorder, and MMPs are highly expressed in AAA lesions. Large numbers of periodontopathic bacteria have been reported to be present in specimens obtained from the aortic walls of patients with an AAA. The purpose of this study was to analyze the influence of periodontopathic bacteria on AAA dilatation.</p>
<p>
<hi rend="bold">Material and Methods: </hi>
AAAs were produced in mice by the periaortic application of 0.25 
<hi rend="smallCaps">m</hi>
CaCl
<hi rend="subscript">2</hi>
, and NaCl was used as a control. The mice were inoculated once weekly with live
<hi rend="italic">Porphyromonas gingivalis</hi>
, live
<hi rend="italic">Aggregatibacter actinomycetemcomitans</hi>
or vehicle.</p>
<p>
<hi rend="bold">Results: </hi>
Four weeks after the periaortic application of either CaCl
<hi rend="subscript">2</hi>
or NaCl, a significant increase was observed in the aortic diameter of
<hi rend="italic">P. gingivalis</hi>
‐challenged mice compared with the vehicle control mice (
<hi rend="italic">p </hi>
<
<hi rend="italic"></hi>
0.05), whereas there was no statistically significant increase in the aortic diameter of the
<hi rend="italic">A. actinomycetemcomitans</hi>
‐challenged mice. Immunohistochemical analysis found significantly higher numbers of CD8‐positive and MOMA2‐positive cells and significantly higher levels of MMP‐2 in the aneurysmal samples of
<hi rend="italic">P. gingivalis</hi>
‐challenged mice compared with control mice. Live
<hi rend="italic">P. gingivalis</hi>
promoted a significant proliferation of splenocytes in comparison with
<hi rend="italic">P. gingivalis</hi>
‐lipopolysaccharide and live
<hi rend="italic">A. actinomycetemcomitans</hi>
(
<hi rend="italic">p </hi>
< 0.05).</p>
<p>
<hi rend="bold">Conclusion: </hi>
These findings demonstrate that challenge with
<hi rend="italic">P. gingivalis</hi>
, but not with
<hi rend="italic">A. actinomycetemcomitans</hi>
, can accelerate, or even initiate, the progression of experimental AAA through the increased expression of MMPs.</p>
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<correspondenceTo>Mitsuaki Isobe, MD, PhD, Department of Cardiovascular Medicine, Tokyo Medical and Dental University, 1‐5‐45 Yushima, Bunkyo‐ku, Tokyo 113‐8549, Japan
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e‐mail:
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<p>
<i>Aoyama N, Suzuki J, Wang D, Ogawa M, Kobayashi N, Hanatani T, Takeuchi Y, Izumi Y, Isobe M.</i>
Porphyromonas gingivalis
<i>promotes murine abdominal aortic aneurysms via matrix metalloproteinase‐2 induction. J Periodont Res 2011; 46: 176–183. © 2010 John Wiley & Sons A/S</i>
</p>
<p>
<b>Background and Objective: </b>
Abdominal aortic aneurysm (AAA) is a common and lethal disorder, and MMPs are highly expressed in AAA lesions. Large numbers of periodontopathic bacteria have been reported to be present in specimens obtained from the aortic walls of patients with an AAA. The purpose of this study was to analyze the influence of periodontopathic bacteria on AAA dilatation.</p>
<p>
<b>Material and Methods: </b>
AAAs were produced in mice by the periaortic application of 0.25 
<sc>m</sc>
CaCl
<sub>2</sub>
, and NaCl was used as a control. The mice were inoculated once weekly with live
<i>Porphyromonas gingivalis</i>
, live
<i>Aggregatibacter actinomycetemcomitans</i>
or vehicle.</p>
<p>
<b>Results: </b>
Four weeks after the periaortic application of either CaCl
<sub>2</sub>
or NaCl, a significant increase was observed in the aortic diameter of
<i>P. gingivalis</i>
‐challenged mice compared with the vehicle control mice (
<i>p </i>
<
<i></i>
0.05), whereas there was no statistically significant increase in the aortic diameter of the
<i>A. actinomycetemcomitans</i>
‐challenged mice. Immunohistochemical analysis found significantly higher numbers of CD8‐positive and MOMA2‐positive cells and significantly higher levels of MMP‐2 in the aneurysmal samples of
<i>P. gingivalis</i>
‐challenged mice compared with control mice. Live
<i>P. gingivalis</i>
promoted a significant proliferation of splenocytes in comparison with
<i>P. gingivalis</i>
‐lipopolysaccharide and live
<i>A. actinomycetemcomitans</i>
(
<i>p </i>
< 0.05).</p>
<p>
<b>Conclusion: </b>
These findings demonstrate that challenge with
<i>P. gingivalis</i>
, but not with
<i>A. actinomycetemcomitans</i>
, can accelerate, or even initiate, the progression of experimental AAA through the increased expression of MMPs.</p>
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<abstract>Aoyama N, Suzuki J, Wang D, Ogawa M, Kobayashi N, Hanatani T, Takeuchi Y, Izumi Y, Isobe M. Porphyromonas gingivalis promotes murine abdominal aortic aneurysms via matrix metalloproteinase‐2 induction. J Periodont Res 2011; 46: 176–183. © 2010 John Wiley & Sons A/S</abstract>
<abstract>Background and Objective:  Abdominal aortic aneurysm (AAA) is a common and lethal disorder, and MMPs are highly expressed in AAA lesions. Large numbers of periodontopathic bacteria have been reported to be present in specimens obtained from the aortic walls of patients with an AAA. The purpose of this study was to analyze the influence of periodontopathic bacteria on AAA dilatation.</abstract>
<abstract>Material and Methods:  AAAs were produced in mice by the periaortic application of 0.25 m CaCl2, and NaCl was used as a control. The mice were inoculated once weekly with live Porphyromonas gingivalis, live Aggregatibacter actinomycetemcomitans or vehicle.</abstract>
<abstract>Results:  Four weeks after the periaortic application of either CaCl2 or NaCl, a significant increase was observed in the aortic diameter of P. gingivalis‐challenged mice compared with the vehicle control mice (p < 0.05), whereas there was no statistically significant increase in the aortic diameter of the A. actinomycetemcomitans‐challenged mice. Immunohistochemical analysis found significantly higher numbers of CD8‐positive and MOMA2‐positive cells and significantly higher levels of MMP‐2 in the aneurysmal samples of P. gingivalis‐challenged mice compared with control mice. Live P. gingivalis promoted a significant proliferation of splenocytes in comparison with P. gingivalis‐lipopolysaccharide and live A. actinomycetemcomitans (p < 0.05).</abstract>
<abstract>Conclusion:  These findings demonstrate that challenge with P. gingivalis, but not with A. actinomycetemcomitans, can accelerate, or even initiate, the progression of experimental AAA through the increased expression of MMPs.</abstract>
<subject lang="en">
<genre>keywords</genre>
<topic>animal model</topic>
<topic>matrix metalloproteinase</topic>
<topic>inflammation</topic>
<topic>Porphyromonas gingivalis</topic>
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<identifier type="ISSN">0022-3484</identifier>
<identifier type="eISSN">1600-0765</identifier>
<identifier type="DOI">10.1111/(ISSN)1600-0765</identifier>
<identifier type="PublisherID">JRE</identifier>
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<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>46</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>2</number>
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<extent unit="pages">
<start>176</start>
<end>183</end>
<total>8</total>
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<identifier type="ark">ark:/67375/WNG-TNZRST69-D</identifier>
<identifier type="DOI">10.1111/j.1600-0765.2010.01326.x</identifier>
<identifier type="ArticleID">JRE1326</identifier>
<accessCondition type="use and reproduction" contentType="copyright">© 2010 John Wiley & Sons A/S</accessCondition>
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