A20誘導による肺上皮細胞におけるアレルギーに対する農場粉塵と内毒素の保護

Martijn J Schuijs¹, Monique A Willart¹, Karl Vergote¹

¹Laboratory of Immunoregulation, VIB Inflammation Research Center, Ghent, Belgium. Department of Internal Medicine, Ghent University, Ghent, Belgium.

Science (New York, N.Y.)

|September 5, 2015

まとめ

牛乳農場で育つことで子どものアレルギーや喘息を防ぐことができます農場環境におけるエンドトキシン (バクテリアのリポポリサカリド) に曝露すると,A20酵素が活性化し,アレルギー反応を防ぐ.

科学分野:

免疫学
環境健康
アレルギー研究

背景:

牛乳農場で育った子どもはアレルギー,花粉症,喘息の割合が低い.
エンドトキシンに富んだ農場環境に関連したアレルギーに対する保護メカニズムは不明である.

研究の目的:

農場環境が喘息のようなアレルギー性疾患に対する保護を与えるメカニズムを調査する.
アレルゲンに対する免疫反応を調節するエンドトキシンと特定の酵素の役割を特定する.

主な方法:

マウスを慢性的に低用量エンドトキシンまたは農場塵にさらし,家粉虫 (HDM) 誘発性喘息に対する保護を評価した.
研究では,内毒素が上皮細胞のサイトカイン生成と樹状細胞 (DC) の活性化に及ぼす影響を調べました.
肺上皮質におけるユビキチン修正酵素A20の役割は,遺伝子ノックアウトモデルで調査された.

主要な成果:

HDM誘発性喘息から保護されたマウスを,エンドトキシンや農場塵に慢性的に曝露させた.
エンドトキシンは,DCを活性化する上皮細胞のサイトカインを減少させ,2型免疫を抑制した.
肺上皮質のA20欠乏は,内毒素の保護効果を無効にしました.
A20遺伝子の単核酸多型化は,農場環境の子供におけるアレルギーと喘息のリスクと相関しています.

結論:

養殖環境は,A20誘導を介して上皮細胞とDC通信を調節することにより,アレルギーから保護します.
A20は,環境内毒素の暴露による喘息発症に対する保護効果を媒介する上で重要な役割を果たします.
発見はアレルギー疾患の予防と治療のための新しい治療目標を示唆しています.

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