第94回日本細菌学会総会

講演情報

ワークショップ

[WS7] 選抜ワークショップ:病原因子と生態防御(毒素・エフェクター・生理活性物質等)

2021年3月24日(水) 16:00 〜 18:00 チャンネル4

コンビーナー:西川 喜代孝(同志社大学),田端 厚之(徳島大学)

[WS7-8/ODP-126] 腸管出血性大腸菌の志賀毒素産生における酸素の影響

○清水 健1,大貫 真奈美1,松本 明郎2,濱端 崇3 (1千葉大学・大学院医学研究院・病原細菌制御学,2東邦大学・医学部・加齢薬理学,3独立行政法人国立国際医療研究センター研究所・感染症制御研究部・細菌感染研究室)

The pathogenesis of EHEC infections is associated with the production of Shiga toxins (Stxs). Stxs produced by EHEC include Stx1 and Stx2. Following the ingestion of contaminated food, EHEC enters the gastrointestinal tract and is released into the intestine. The environment of the intestinal tract is characterized by variable oxygen levels. EHEC might sense change in oxygen availability and switch from anaerobiosis to microaerobiosis. We investigated the impact of O2 availability on Stxs production. The change from anaerobiosis to microaerobiosis enhanced the magnitude of both Stxs production. In E. coli, oxygen-regulated expressions of the metabolic enzymes are affected by the ArcA and Fnr. Thus, we confirmed whether ArcA and Fnr were related with increased Stxs production in change from anaerobic to microaerobic conditions. As a result, increased Stx2 production under microaerobic conditions was dependent on the Fnr. Recently, it was reported that the lack of O2 changes the expression of genes controlled by Fur. Moreover, the stx1 promoter region represents the functional Fur-binding site. Thus, we confirmed whether Fur was dependent on increased Stx1 production when the environment was changed from anaerobic to microaerobic conditions. As a result, increased Stx1 production under microaerobic conditions could explain the Fur-mediated repression of the stx1 promoter.