| Project/Area Number |
15K20597
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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 |
Orthodontics/Pediatric dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
IWASA Akihiko 徳島大学, 大学院医歯薬学研究部(歯学系), 助教 (90746025)
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| Research Collaborator |
TANAKA Eiji
IZAWA Takashi
SATO Minami
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 慢性炎症 / アロマターゼ / シェーグレン症候群 |
|---|
| Outline of Final Research Achievements |
The mechanism by which estrogen deficiency influences autoimmunity is unknown. Aromatase is a converting enzyme from androgens to estrogens. In the present study, we used female aromatase gene knockout (ArKO) mice as a model of estrogen deficiency to investigate the molecular mechanism that underlies the onset and development of autoimmunity. Histological analyses showed that inflammatory lesions in the lacrimal and salivary glands of ArKO mice increased with age. Expression of mRNA encoding proinflammatory cytokines and monocyte chemotactic protein-1 (MCP-1) increased in white adipose tissue (WAT) of ArKO mice and was significantly higher than that in wild-type mice. Moreover, an increased number of inflammatory M1-macrophages was observed in WAT and salivary glands of ArKO mice. These results suggest that adiposity in the target organ may disrupt peripheral immune tolerance leading to the development of autoimmunity.
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