2018 Fiscal Year Final Research Report
The development of prevention and treatemnt methods of fertilization failure from mice model
| Project/Area Number |
17K19324
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Veterinary medical science, Animal science, and related fields
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Research Collaborator |
Miyamoto Akio
Imakawa Kazuhiko
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| Project Period (FY) |
2017-06-30 – 2019-03-31
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| Keywords | 子宮 / 卵管 / 精子 / 免疫機構 |
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| Outline of Final Research Achievements |
Sperm are non-self for female; however, sperm are ejaculated to uterus for fertilization. To remove the extra sperm in uterus and pass the fertilizing sperm to oviduct, uterus has the specific immune condition where uterus epithelial cells express TLR2 and TLR4. The stimuli activate p38MAPK and JNK but not NFkB to induce the AP-1-regulating gene expression, including chemokine family. The secreted chemokines recrute leucocytes that remove the extra sperm by phagocytosis. The linier motility sperm that have the high transcription and translational activities in mitochondria can transfer to oviduct for fertilization. If the mechanisms were affected by unphysiological factors, such as infections, sperm could not pass to oviduct or the serious inflammation would attack the early embryo transferred from oviduct. Therefore, the basic information about immune functions in uterus are contributed for infertility care and increase the performance of reproductive technology.
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| Free Research Field |
家畜繁殖学
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| Academic Significance and Societal Importance of the Research Achievements |
子宮内に精子が残存することは，雌にとって異物である精子に対する抗体が産生される要因となる．また，除去するために細胞性免疫が活性化しすぎると子宮内は炎症状態となり，受精卵も攻撃対象となってします．このような免疫寛容と炎症のバランスを保つ仕組みとして，子宮上皮細胞によるTLR2とTLR4系の制御機構を理解することで，精子抗体や着床異常の原因探索が可能となると期待される．さらに，人工授精時の子宮内免疫環境の把握が可能となり，繁殖成績向上に寄与するものである．
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