ハイパーウイルス性の結核菌株のグリコリピドで,先天的な免疫反応を抑制する
Michael B Reed1, Pilar Domenech, Claudia Manca
1Tuberculosis Research Section, NIAID, National Institutes of Health, 12441 Parklawn Drive, Rockville, Maryland 20852, USA.
Nature
|September 3, 2004
まとめ
マイコバクテリウム結核フェノールグリコリピド (PGL) は,マウスの高死亡率に寄与する. PGLの合成を妨害すると,ウイルス性が低下し,PGLは免疫細胞からの炎症性サイトカインの放出を抑制する.
科学分野:
- 結核に関する研究.
- 免疫学 免疫学とは
- 微生物の病原性が生成する.
背景:
- 結核 (TB) は,毎年何百万もの死者を引き起こす世界的な健康上の大きな脅威であり続けています.
- 遺伝的類似性にもかかわらず,Mycobacterium tuberculosis菌株はさまざまな臨床結果を示しています.
- 細菌因子による宿主免疫応答の修正は,結核病原性の鍵である.
研究 の 目的:
- ハイパーウイルス性のM. tuberculosis株における生物学的に活性な脂質種を特定し,特徴づけること.
- この脂質が病気の病原性および宿主免疫反応における役割を調査する.
主な方法:
- ポリケチド合成酵素由来フェノールグリコリピド (PGL) の特定 W-北京 M. tuberculosisの単離体.
- M. tuberculosis.におけるPGL合成の遺伝的障害である.
- バクテリアの負荷と高致死性を評価するためのマウイン感染モデル.
- モノサイト由来マクロファージを用いたインビトロ研究で,サイトカインの放出量を測定した.
主要な成果:
- M. tuberculosis (W-北京ファミリー) のサブセットは,PGL.に関連した高毒性フェノタイプを生成する.
- PGL合成の障害は,バクテリアの負荷を変えることなく,ネズミのモデルで高死亡率を廃止しました.
- PGLの減少は,炎症誘発性サイトカイン (TNF-α,IL-6,IL-12) の放出の増加と相関する.
- PGLは,マクロファージからの炎症誘発性サイトカインの放出を,投与量に依存した方法で抑制した.
結論:
- フェノルグリコリピド (PGL) は,超致死性Mycobacterium tuberculosis菌株における重要な毒性因子である.
- PGLは,炎症性サイトカインの産生を抑制することによって宿主の免疫反応を調節する.
- PGLの合成や機能をターゲットにすることで,結核治療の新たな戦略を提示することができる.
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