S100A8/A9アラルミンの活性化により,馬の昇進性胎盤炎における炎症経路が強化される
Kirsten E Scoggin1, Shimaa I Rakha2, Ahmed M Abdellatif3
1Maxwell H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546, USA.
International journal of molecular sciences
|February 13, 2026
まとめ
S100A8 / S100A9 (S100A8 / A9) アラルミンは,急性および慢性馬の胎盤炎の両方でアップ調節され,炎症と組織損傷を引き起こします. このS100A8/A9経路をターゲットにすると,妊娠中絶の治療の可能性が生まれます.
科学分野:
- 獣医免疫学 獣医免疫学について
- 生殖免疫学 生殖免疫学
- 馬の病理学についてです.
背景:
- アセンディング胎盤炎は,馬の妊娠中絶の主な原因です.
- 馬の胎盤炎の上流の炎症的トリガーは,まだ十分に理解されていません.
- S100A8/S100A9 (S100A8/A9) のアラルミンは,以前,慢性モデルにおいて,潜在的な上流調節体として特定されていた.
研究 の 目的:
- S100A8 / A9のアップレギュレーションが急性馬胎盤炎および臨床症例で持続するかどうかを判断するために.
- S100A8/A9経路における下流炎症媒介者の発現を調査する.
- 馬の胎盤炎におけるS100A8/A9信号軸の役割を明らかにする.
主な方法:
- 実験的な急性および慢性胎盤炎モデルにおけるS100A8/A9 mRNA発現の定量化.
- 胎盤組織におけるS100A8/A9タンパク質の局所化を検出するための免疫ヒストケミストリー.
- 臨床性胎盤炎症例のRNA配列分析により,下流の炎症媒介体および受容体を特定する.
主要な成果:
- S100A8およびS100A9のmRNA発現は,急性および慢性馬胎盤炎の両方において著しく上調されました.
- S100A8 / A9タンパク質は,胎盤炎組織に中性粒子が密集して浸透しました.
- 臨床症例では,S100A8/A9受容体 (TLR4,RAGE) とNF-κB誘発の炎症媒介体 (IL1β,IL6,TNF,CXCL8,CCL2,CXCL10,CASP3) の同時上調が示されました.
結論:
- S100A8 / A9のアップレギュレーションは,慢性病理に限定されない,馬の胎盤炎の持続的な特徴です.
- 一貫したS100A8/A9-TLR4/RAGE-NF-κBシグナリング軸は,臨床馬胎盤炎における炎症と組織損傷を誘導する.
- S100A8/A9アラミンには診断の可能性があり,馬の感染症による妊娠中絶を緩和するための有望な治療目標です.
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