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KAKEN_24591488seika.pdf
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重症感染症におけるPGD2/CRTH2を介する免疫機構の解明
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ジュウショウ カンセンショウ ニ オケル PGD2/CRTH2 オ カイスル メンエキ キコウ ノ カイメイ
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Jusho kansensho ni okeru PGD2/CRTH2 o kaisuru meneki kiko no kaimei
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Investigation of immune mechanism of PGD2/CRTH2 in severe infectious diseases
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石井, 誠
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イシイ, マコト
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Ishii, Makoto
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慶應義塾大学・医学部・専任講師
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Research team head
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科研費研究者番号 : 30317333
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藤猪, 英樹
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フジイ, ヒデキ
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Fujii, Hideki
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琉球大学・医学研究科・准教授
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Research team member
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科研費研究者番号 : 50356250
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2015
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科学研究費補助金研究成果報告書
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2014
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敗血症におけるCRTH2の役割を検討した。CRTH2ノックアウト(-/-)マウスは, 敗血症において生存率が上昇し, 腹腔内の細菌数は有意に減少した。CRTH2-/-マウスは, 腹腔内のCXCR2陽性の好中球が増加した。好中球マーカーであるGr-1の抗体や, CXCR2抗体の投与実験の結果, CRTH2-/-マウスの保護的効果の機序にCXCR2陽性の好中球の腹腔内への集積が寄与していた。感染2時間後の末梢好中球のCXCR2プロモーター領域のヒストンH3のアセチル化は, 野生型では低下するが, CRTH2-/-マウスでは低下せず, CXCR2の発現はエピジェネティック制御を受けることが示唆された。
We evaluated the role of CRTH2 using a mice model of polymicrobial sepsis. CRTH2 knockout (-/-) mice were highly resistant to sepis and peritoneal bacterilal load in CRTH2-/- mice was significantly lower as compared to that in wild-type mice.Pharmacological inhibition of Gr-1, a neutrophil marker, and CXCR2 attenuated the protective effects aganist sepsis in CRTH2-/- mice, indicating that CXCR2-expressing neutrophils play protective roles in CRTH2-/- mice in this sepsis model. Moreover, acetylation of histone H3 at CXCR2 promoter in perippheral neutrophils was reduced 2 h after the surgery in wild-type neutrophils, while that in CRTH2-/- mice was not reduced 2 h after the surgery, suggesting that CXCR2 expression is regulated by epigenetic change.
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研究種目 : 基盤研究(C)
研究期間 : 2012～2014
課題番号 : 24591488
研究分野 : 感染免疫学
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