嚢胞性線維症（CF）はCFTRクロライドチャンネルの機能不全により発症することがわかっている。現在はCFTR分子の移動や機能を補助する薬剤が開発され、また遺伝子治療も試みられ、少しづつ原因分子に対する治療が進んでいる。この病気が肺だけでなく全身性の病気であることを考えると、内服でCFTRの機能を助ける方法は期待できるが、その価格は１年間で３０００万円と極めて高額で、いつもなんとかならないかと思う。

ただ、この病気で最も辛い症状は肺の感染症で、特に緑膿菌の感染は厄介な問題だ。痰のキレをスムースにするためにDNase Iが効果があり、症状軽減に大きく貢献しているが、感染に対しては決定的対応ができていない。

なぜ緑膿菌感染がCFで多いのか？単純にクロライドチャンネル異常による粘液分泌上昇のせいかと考えていたが、今日紹介するジュネーブ大学からの論文はCFの気道が特に緑膿菌が接着しやすい性質を持つことが感染が起こりやすい原因である可能性を示唆している。タイトルは「Vav3 Mediates Pseudomonas aeruginosa Adhesion to the Cystic Fibrosis Airway Epithelium （VAV3は嚢胞性線維症の気道上皮への接着を媒介する）」だ。

この研究ではまず患者さんの気道上皮と正常人の気道上皮の遺伝子発現を比較し、患者さんでは細胞接着に関わるβ1インテグリンとファイブロネクチンの発現とともに、GDP/GTPの変換に関わるVAV3と呼ばれる分子の発現も高まっていることを発見する。この発見が研究のすべてで、あとはここから緑膿菌の感染までどのようなシナリオが成立するかになる。

詳細を省いて、最終的シナリオだけを紹介すると次のようになる。

• CFTR機能不全によりVAV３の発現が高まる。
• VAV3はGタンパク質の一つCDC42を調節して細胞骨格を再構成させる。
• VAV3はインテグリンとファイブロネクチンの気道内への分泌を調節している。
• CFの気道細胞でも、VAV3をノックダウンすると、構造は正常化する。
• CFで分泌が高まっている粘液によりファイブロネクチンは分解され、この分解産物が緑膿菌を結合する。
• 試験管内実験系だが、CFの上皮のVAV3をノックダウンすると緑膿菌の接着が抑えられる。

以上がシナリオで、納得のできる説明だと思う。問題は実際の気道で緑膿菌の接着や感染が防げるかについてのデータが示されないため、論文としてはフラストレーションが残った。とはいえ、VAV3の阻害剤の吸入、あるいはインテグリン分解産物と緑膿菌の接着を阻害する分子の吸入が開発できれば、この病気の治療はさらに前進するように感じた。

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