細胞外細菌の病原体は宿主の代謝を調節して,自身の感知と増殖を調節する
Moshe Baruch1, Ilia Belotserkovsky1, Baruch B Hertzog1
1Department of Microbiology and Molecular Genetics, The Hebrew University of Jerusalem, Faculty of Medicine, Jerusalem 91120, Israel.
Cell
|January 21, 2014
まとめ
グループA型ストレプトコッカス (GAS) 感染症は,栄養素の吸収に依存しています. バクテリアは宿主によって放出されたアスパラジン (ASN) を感知し,遺伝子発現と毒性を変化させ,治療目標を提供します.
科学分野:
- 微生物学 微生物学とは
- 感染症 感染症は感染症です.
- 分子生物学は分子生物学である.
背景:
- グループA型ストレプトコッカス (GAS) は,ヒトの重要な病原体です.
- 栄養素の獲得は,細菌の生存と感染症の進行に不可欠です.
- GASと宿主の相互作用を理解することは,効果的な治療法の開発に不可欠です.
研究 の 目的:
- GASの病原性におけるアスパラジン (ASN) の役割を明らかにする.
- ASNによって規制されたGASの毒性因子を特定するために.
- GAS感染に対する潜在的な治療目標としてASN代謝を調査する.
主な方法:
- GAS.のリポーターとして,クオラムセンシングのSILシステムを活用しました.
- 宿主細胞とGASの相互作用と毒素の配送を調査した.
- 分析された遺伝子発現の変化は,ASNに対する反応である.
- アスパラギナーゼがGASの成長に与える影響を in vitroおよびin vivoで評価した.
主要な成果:
- GASはストレプトリシン毒素を放出し,宿主細胞のエンドプラズマ網膜のストレスを誘発する.
- ホスト細胞のストレスは,GASが感知するASNの生成を高めます.
- ASNはGAS遺伝子の約17%の発現に影響を与え,ストレプトリシン毒素のアップレギュレーションと増殖遺伝子のダウンレギュレーションを含む.
- アスパラギナゼは,ヒトの血液とマウスバクテリーミアモデルのGAS増殖を効果的に抑制します.
結論:
- GASは,宿主細胞のストレス反応を操作することによって,栄養素を取得するための洗練されたメカニズムを使用します.
- ASNは,GASにおける重要なシグナル伝達分子として作用し,ウイルス性因子の発現を調節します.
- アスパラギナーゼによるASN代謝をターゲットにすることは,GAS感染症に対する有望な治療戦略です.
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