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KAKEN_15K09580seika.pdf
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Download
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:345.5 KB
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:Nov 12, 2018 |
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Total downloads since Nov 12, 2018 : 314
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重症感染症の新たな治療戦略確立に向けたエピジェネティック制御機構の解明
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ジュウショウ カンセンショウ ノ アラタナ チリョウ センリャク カクリツ ニ ムケタ エピジェネティック セイギョ キコウ ノ カイメイ
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Jūshō kansenshō no aratana chiryō senryaku kakuritsu ni muketa epijenetikku seigyo kikō no kaimei
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Elucidation of epigenetic gene regulation mechanism for establishment of new therapeutic strategies for 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(信濃町)・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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中山, 俊憲
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ナカヤマ, トシノリ
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Nakayama, Toshinori
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千葉大学・医学部免疫発生学教室・教授
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Research team member
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科研費研究者番号 : 50237468
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八木, 一馬
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ヤギ, カズマ
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Yagi, Kazuma
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2018
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科学研究費補助金研究成果報告書
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2017
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本研究は重症インフルエンザ感染後肺炎球菌性肺炎にヒストンアセチル化を介したエピジェネティクス制御が関与している仮説のもとに, C57BL/6マウスにインフルエンザA(PR8株)5PFUを点鼻投与し, 7日後に10の4乗CFUの肺炎球菌を点鼻感染させた。ヒストン脱アセチル化酵素(HDAC)阻害薬のTSAを1日1回腹腔内投与を行った(1mg/kg)ところ, HDAC活性は有意に低下し, 生存率も有意に向上し, 細菌の菌量や肺胞洗浄液中の総細胞数は有意に低下した。さらにTSA投与により全肺NK細胞数も有意に低下し, TSAによるインフルエンザ感染後肺炎球菌性肺炎の保護的効果に寄与している可能性が考えられた。
The hypothesis of the study was epigenetic mechanism, especially for histone acetylation, might contribute to the poor outcome of post-influenza pneumonia. Mice were infected intranasally with 1.0×104 CFU of Streptococcus pneumoniae 7 days after intranasal inoculation with 5 PFU of influenza virus A/PR8.The mice were intraperitoneally injected with the histone deacetylase (HDAC) inhibitor TSA. TSA significantly suppressed HDAC activity and significantly improved the survival rate of mice after post-influenza pneumococcal infection, which was associated with a significant decrease in bacterial load and the total cell count of the BALF. The number of natural killer cells in the lungs were significantly lower in the TSA-treated group, which may contribute to the protective effects of TSA.
TSA protects mice against post-influenza pneumococcal pneumonia possibly through multiple factors, including a decrease in lung and systemic bacterial load, and suppression of systemic inflammation.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2015～2017
課題番号 : 15K09580
研究分野 : 呼吸器内科学
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