The 94th Annual Meeting of Japanese Society for Bacteriology

Presentation information

Workshop

[WS7] Selected from Oral Session: Virulence Factors and Biophylaxis: Toxins, Effectors, Bioactive substances

Wed. Mar 24, 2021 4:00 PM - 6:00 PM Channel 4

Conveners: Kiyotaka Nishikawa (Doshisha University), Atsushi Tabata (Tokushima University)

[WS7-8/ODP-126] Effect of O2 availability on Stx1 and Stx2 productions in enterohemorrhagic Escherichia coli

○Takeshi Shimizu1, Manami Onuki1, Akio Matsumoto2, Takeshi Hamahata3 (1Dept. Molecular Infectiology, Grad. Sch. Medicine, Chiba Univ., 2Dept. Aging Pharmacology, Sch. Medicine, Toho Univ., 3Section of Bacterial Infection, Research Institute, National Center for Global Health and Medicine)

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.