| Project/Area Number |
13671932
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Tohoku University (2002)
Kyushu Dental College (2001) |
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Principal Investigator |
KOSEKI Takeyoshi Tohoku University Graduate School of Dentistry, Department of Oral Health and Development Sciences, Professor, 大学院・歯学研究科, 教授 (80291128)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Periodontal Disease / Intracellular Invasion / Apoptosis / Actinobacillus actinomycetemcomitans / Legionellapneumophila / 歯周病疾患 |
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| Research Abstract |
Actinobacillus actinomycetemcomitans is a Gram-negative, capnophilic coccobacillus which has been considered to be an etiologic agent especially in the severe form of juvenile and adult periodontitis. Previous studies suggested that A.actinomycetemcomitans can invade into periodontal tissues of advanced periodontitis and then survive inside the host cells. We previously showed that apoptotic cell death of the marine macrophage-like cell line was induced by A. actinomycetemcomitans infection. During the course of this apoptosis, activation of several caspases was observed. In general medicine, the facts that severl important pathogenic bacteria can infect and multiple inside the host cells and cause the severe life-threaten infection has been reported. Intracellular invasion mechanisms of some pathogenic bacteria were analyzed in detail, and several caspases has been reported to activate during the course of invasion. We hypothesized that Legionella pneumophila, which causes legion dise
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ase, and periodontopathic bacteria, A.actinomycetemcomitans, might invade inside the host cells in similar manner, because both target macrophaees to invade and activate similar set of caspases in host cells. We first adapted the invasion assay designed for A. actinomycetemcomitans to that for L. pneumphila. Mouse macrophage cell line J744.1 and mouse monocyte cell line RAW264.7 are both showed to induce cell death by infection of these bacteria. However, the cell death cased by L. pneumophila was necrosis because the content of cell is filled with multipled bacterial cells just before cell explosion. The difference of the cell death caused by each bacterium might depended on the different signal pathway which are activated by infection even if the similar set of caspases was activated. The RAW264.7 cells which constitutively expressed anti-apopotic Bcl-2 or Bcl-x_L did not rescue cell death by the infection of A. actinomycetemcomitans. Considering all, the mechanisms of invasion and infection of A. actinomycetemcomitans is unique and we need further analysis of these mechanisms for preventing periodontal diseases. Less
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