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

Abstract

The qseBC-encoded quorum-sensing system regulates the motility of Escherichia coli O157:H7 in response to bacterial autoinducer 3 (AI-3) and the mammalian stress hormones epinephrine (E) and norepinephrine (NE). The qseC 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 of E. coli O157:H7 and its isogenic qseBC mutant showed significantly higher fecal shedding of the qseBC mutant. In vitro analysis revealed similar growth profiles and motilities of the qseBC mutant and the parental strain in the presence or absence of NE. The magnitudes of the response to NE and expression of flagellar genes flhD and fliC were also similar for the qseBC mutant and the parental strain. The expression of ler (a positive regulator of the locus of enterocyte effacement [LEE]), the ler-regulated espA gene, and the csgA gene (encoding curli fimbriae) was increased in the qseBC mutant compared to the parental strain. On the other hand, growth, motility, and transcription of flhD, fliC, ler, espA, and csgA were significantly reduced in the qseBC mutant complemented with a plasmid-cloned copy of the qseBC 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 the qseBC mutant in calves.

Beyond a ribosomal RNA methyltransferase, the wider role of MraW in DNA methylation, motility and colonization inEscherichia coliO157:H7

“…coli (42). The decreased colonization by the mraW mutant is less likely due to reduction of motility as less or non-motile E. coli O157:H7 was preferred in the animal intestine including mice (11, 43).…”

Peer Review #2 of "QseBC is involved in the biofilm formation and antibiotic resistance in Escherichia coli isolated from bovine mastitis (v0.1)"

“…However, Gou et al showed that the absence of qseB resulted in increased bacterial motility but no obvious differences in biofilm formation in E. coli MG1655 (Gou et al 2019). In addition, our results of RT-qPCR showed that inactivation of qseBC resulted in an apparent decrease in the transcript levels of bcsA, csgA, fliC, motA, wcaF and fimA, whereas Sharma and Casey reported that QseBC did not affect the transcription of fliC, and inactivation of qseBC upregulated the transcription of csgA in EHEC O157:H7 (Sharma & Casey 2014). These conflicting results were probably due to the isolation of these E.coli strains from different hosts, and thus the biofilm formation ability and the regulatory mechanisms of biofilm formation might differ between them.…”

“…Two-component systems are essential for bacteria to quickly respond and adapt to various environmental stimuli, particularly through changes in target gene transcription (Beier & Gross 2006). In the QseBC two component system, the environmental signal bacterial autoinducer 3 (AI-3) and the mammalian stress hormones epinephrine and norepinephrine (Clarke et al 2006;Hughes et al 2009;Sharma & Casey 2014) are sensed by QseC (an inner membrane-bound sensor histidine kinase (HK)), which initiates a signal transduction cascade that, in many cases, results in the phosphorylation of aspartate residue of QseB (the response regulator (RR)) (Hoch & Varughese 2001;Weigel & Demuth 2016). QseB regulates the transcription of downstream target genes.…”

“…QseBC TCS was first discovered in enterohaemorrhagic Escherichia coli (EHEC) and generally functions as a global regulator of virulence (Weigel & Demuth 2016). Besides, other studies have demonstrated that QseBC TCS contributes to the regulation of colonization, motility and expression of virulence genes in Enterohaemorrhagic Escherichia coli O157:H7 (Clarke & Sperandio 2005b;Sharma & Casey 2014), motility and biofilm formation in Escherichia coli PeerJ reviewing PDF | (2019:10:42311:2:0:NEW 22 Feb 2020)…”

The anti-Salmonella and immunostimulatory properties of yeast-based postbiotics in poultry and cattle

“…coli O157:H7 was enumerated in 100 of the swab samples (five per pen; 50 swab samples per treatment) using selective media (Sorbitol-MacConkey agar) and a PCR targeting E. coli O157:H7 virulence genes as per Sharma and Casey (Sharma and Casey, 2014). Approximately 0.3 gm of feces were transferred into enrichment broth (Sharma and Casey et al, 2014) and an aliquot of the broth was plated on sorbitol-MacConkey agar, incubated overnight at 37 o C, and subjected to enumeration by manual counting of nonfermenting colonies the next day. From each pen-specific set of agar plates, 96 colonies were selected and subjected to the PCR targeting E. coli O157:H7 virulence genes.…”