The 95th Annual Meeting of Japanese Society for Bacteriology

Presentation information

On-demand Presentation

[ODP22] 5. Pathogenicity -b. Toxins, effectors and physically active substances

[ODP-115] Enhanced production of Shiga toxin 2 in enterohemorrhagic Escherichia coli by oxygen

Takeshi Shimizu1, Manami Onuki1, Shinichiro Hirai2, Eiji Yokoyama3, Akio Matsumoto4, Takashi Hamabata5 (1Dept. Mol. Infect., Sch. Med., Chiba Univ., 2Dept. Infect. Dise. Risk Manag. Center, N. I. I. D, 3Div. Bacteriol., Chiba Prefect. Instit. Pub. Heal., 4Dept. Aging Pharmacol., Sch. Med., Toho Univ., 5Sect. Bact. Infect., Re. Inst., Nat. Cen. Glo. Heal. Med.)


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. In fact, increased Stx1 production in the presence of oxygen is dependent on Fur. However, the mechanism of oxygen sensing for the regulation of Stx2 production in EHEC remains unknown. Thus, we investigated the impact of O2 availability on Stx2 production. The change from anaerobiosis to microaerobiosis enhanced the magnitude of Stx2 production. We confirmed whether Fnr were related with increased Stx2 production in change from anaerobic to microaerobic conditions. As a result, increased Stx2 production under microaerobic conditions was dependent on the Fnr. However, the regulation of Fnr in the presence of oxygen is required for unknown EHEC-specific factor(s). The sensitivity to react to oxygen of PStx1 activity was higher than that of the early phage promoter (PL) activity of the Stx2-phage. These results suggest that the increase in oxygen concentration may initially enhance Stx1 production and subsequently induce Stx2 production in EHEC.