Abstract
Enterohemorrhagic Escherichia coli (EHEC) produces Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2). Nitric oxide (NO), which acts as an antimicrobial defense molecule, was found to enhance the production of Stx1 and Stx2 in EHEC under anaerobic conditions. Although EHEC O157 has two types of anaerobic NO reductase genes, an intact norV and a deleted norV, in the deleted norV‐type EHEC, a high concentration of NO (12–29 μmol/L, maximum steady‐state concentration) is required for enhanced Stx1 production and a low concentration of NO (~12 μmol/L, maximum steady‐state concentration) is sufficient for enhanced Stx2 production under anaerobic conditions. These results suggested that different concentration thresholds of NO elicit a discrete set of Stx1 and Stx2 production pathways. Moreover, the enhancement of Shiga toxin production in the intact norV‐type EHEC required treatment with a higher concentration of NO than was required for enhancement of Shiga toxin production in the deleted norV‐type EHEC, suggesting that the specific NorV type plays an important role in the level of enhancement of Shiga toxin production in response to NO. Finally, Fur derepression and RecA activation in EHEC were shown to participate in the NO‐enhanced Stx1 and Stx2 production, respectively.
Highlights
Enterohemorrhagic Escherichia coli (EHEC) O157 is a causative agent of intestinal disorders ranging from mild infection to severe, bloody diarrhea (Hofmann, 1993; Keusch & Acheson, 1997; Lansbury & Ludlam, 1997)
We found that enhanced Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2) production in response to Nitric oxide (NO) was involved in Fur derepression and RecA activation in EHEC O157, respectively
To further confirm the ability of NO in the deleted norV-type EHEC to enhance Stx1 and Stx2 production, we examined the effects of other NO donors and an inactive NO donor on Shiga toxin production under anaerobic conditions
Summary
Enterohemorrhagic Escherichia coli (EHEC) O157 is a causative agent of intestinal disorders ranging from mild infection to severe, bloody diarrhea (hemorrhagic colitis) (Hofmann, 1993; Keusch & Acheson, 1997; Lansbury & Ludlam, 1997). The pentamer of B subunits binds to the surface receptor, glycolipid receptor Gb3, on the target cells (Jacewicz, Clausen, Nudelman, Donohue-Rolfe, & Keusch, 1986) Both Shiga toxin genes in EHEC are located within Stx-encoding phages that are related to the λ phage, which is well-characterized with respect to both its genome arrangement and transcription. E. coli has evolved several mechanisms for NO detoxification (Poole, 2005; Spiro, 2006, 2007) It expresses a flavorubredoxin (NorV), which reduces NO to N2O under anaerobic conditions (Gardner, Costantino, & Salzman, 1998; Gardner & Gardner, 2002; Gardner, Helmick, & Gardner, 2002; Spiro, 2012). We found that enhanced Stx and Stx production in response to NO was involved in Fur derepression and RecA activation in EHEC O157, respectively
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