| Project/Area Number |
23792149
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
OKINAGA Toshinori 九州歯科大学, 歯学科・感染分子生物学分野, 助教 (60582773)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 免疫 / 感染 / 炎症 / 歯周病と全身疾患 / 歯周病原性細菌 / クオラムセンシング / 心血管疾患 / マクロファージ / 歯周病原細菌 |
|---|
| Research Abstract |
Atherosclerosis shows a chronic inflammatory process initiated by the recruitment of monocyte-derived macrophage into the sub-endothelial arterial space. Chronic bacterial infections, including periodontitis, are associated with an increased risk of coronary heart diseases. Periodontitis is a chronic inflammatory disease infected with a gram-negative periodontopathic bacterium, such as Aggregatibacter actinomycetemcomitans. We previously reported that infection of murine macrophages in vitro with the periodontopathic bacterium A. actinomycetemcomitans induced cell cycle arrest during phase G1. In the present study, we investigated the role of suppressor of cytokine signaling (SOCS) in induction of the cell cycle in A. actinomycetemcomitans-infected macrophages. Our results indicate that intrinsic SOCS-3 normally activates the expression of cell cycle associated protein, while overexpression of SOCS-3 down-regulates p21 expression in infected RAW 264.7 cells, suggesting that SOCS-3 has dexterous effects to regulate the cell cycle in macrophages infected with periodontopathic bacteria.
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