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TheqseBC -encoded quorum-sensing system regulates the motility ofEscherichia coli O157:H7 in response to bacterial autoinducer 3 (AI-3) and the mammalian stress hormones epinephrine (E) and norepinephrine (NE). TheqseC gene encodes a sensory kinase that autophosphorylates in response to AI-3, E, or NE and subsequently phosphorylates its cognate response regulator QseB. In the absence of QseC, QseB downregulates bacterial motility and virulence in animal models. In this study, we found that 8- to 10-month-old calves orally inoculated with a mixture ofE. coli O157:H7 and its isogenicqseBC mutant showed significantly higher fecal shedding of theqseBC mutant.In vitro analysis revealed similar growth profiles and motilities of theqseBC mutant and the parental strain in the presence or absence of NE. The magnitudes of the response to NE and expression of flagellar genesflhD andfliC were also similar for theqseBC mutant and the parental strain. The expression ofler (a positive regulator of the locus of enterocyte effacement [LEE]), theler -regulatedespA gene, and thecsgA gene (encoding curli fimbriae) was increased in theqseBC mutant compared to the parental strain. On the other hand, growth, motility, and transcription offlhD ,fliC ,ler ,espA , andcsgA were significantly reduced in theqseBC mutant complemented with a plasmid-cloned copy of theqseBC genes. Thus,in vitro motility and gene expression data indicate that the near-parental level of motility, ability to respond to NE, and enhanced expression of LEE and curli genes might in part be responsible for increased colonization and fecal shedding of theqseBC mutant in calves.

applied and environmental microbiology

<i>Escherichia coli</i> O157:H7 Lacking the <i>qseBC</i> -Encoded Quorum-Sensing System Outcompetes the Parental Strain in Colonization of Cattle Intestines

Escherichia coli O157:H7 Lacking the qseBC -Encoded Quorum-Sensing System Outcompetes the Parental Strain in Colonization of Cattle Intestines