バクテリアの小分子によるNF-kappaBシグナル伝達の破壊による遺伝子発現の調節
Vladimir V Kravchenko1, Gunnar F Kaufmann, John C Mathison
1Department of Immunology and Microbial Sciences, Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
まとめ
細菌のN-(3-オクソ-ドデカノイル) ホモセリンラクトン (C12) は,哺乳類における核転写因子NF-kappaBの調節を選択的に阻害する. この細菌分子は免疫遺伝子を抑制し,Pseudomonas aeruginosaのような病原菌が持続的な感染を確立するのを助けます.
科学分野:
- 免疫学 免疫学とは
- 微生物学 微生物学とは
- 分子生物学は分子生物学である.
背景:
- 生まれつきの免疫は,病原菌と戦うために核転写因子NF-kappaBの活性化に依存しています.
- NF-kappaBの調節不良は,免疫不全や慢性炎症につながる可能性があります.
研究 の 目的:
- 哺乳類の細胞におけるNF-kappaB調節に対するバクテリアのN-(3-オクソ-ドデカノイル) ホモセリンラクトン (C12) の影響を調査する.
- C12が先天的な免疫反応と遺伝子発現にどのように影響するかを理解する.
主な方法:
- 活性化された哺乳類の細胞を細菌C12で処理する.
- NF-kappaBの活性化とNF-kappaBに反応する遺伝子発現の分析.
主要な成果:
- 細菌C12は,活性化された哺乳類細胞におけるNF-kappaBの調節を選択的に阻害する.
- C12は,炎症性サイトカインと免疫調節因子をコードする遺伝子の誘導を特に抑制します.
- このメカニズムは,好機的な病原体が先天的な免疫系を回避することを可能にします.
結論:
- バクテリアのC12は,NF-kappaBシグナリングを標的として宿主の先天的免疫を抑制するウイルス性因子です.
- この抑制は,Pseudomonas aeruginosaのような病原体による持続的な感染を容易にし,特にシスティック・フィブロシスなどの状態においてそうである.
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