A central metabolic circuit controlled by QseC in pathogenic <i>Escherichia coli</i>

Hadjifrangiskou, Maria; Kostakioti, Maria; Chen, Swaine L.; Henderson, Jeffrey P.; Greene, Sarah E.; Hultgren, Scott J.

doi:10.1111/j.1365-2958.2011.07660.x

Cited by 113 publications

(167 citation statements)

References 59 publications

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“…2B). These observations confirm that QseC mediates NE's effects on LF82 flagellar expression and motility, with the caveat that NE-induced QseC-signaling has broad effects on bacterial physiology (19).…”

Section: Resultssupporting

confidence: 71%

“…Previous gene expression analysis in WT vs. ΔqseC uropathogenic E. coli strains revealed that qseC deletion results in altered nucleotide, amino acid, and carbon metabolism (19). Observing that LF82 is more adept at persisting in a low-complexity microbiota (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Beyond flagella and their proteins, the virulence of many pathogenic E. coli is dependent on quorum-sensing E. coli regulator C (QseC), a component of the quorum-sensing E. coli regulators B and C (QseBC) two-component system (TCS) (18,19). QseC is Significance Bacteria use two-component quorum-sensing systems to communicate with each other and their hosts.…”

mentioning

confidence: 99%

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QseC inhibition as an antivirulence approach for colitis-associated bacteria

Rooks

Veiga

Reeves

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Hosts and their microbes have established a sophisticated communication system over many millennia. Within mammalian hosts, this dynamic cross-talk is essential for maintaining intestinal homeostasis. In a genetically susceptible host, dysbiosis of the gut microbiome and dysregulated immune responses are central to the development of inflammatory bowel disease (IBD). Previous surveys of stool from the T-bet −/− Rag2 −/− IBD mouse model revealed microbial features that discriminate between health and disease states. Enterobacteriaceae expansion and increased gene abundances for benzoate degradation, two-component systems, and bacterial motility proteins pointed to the potential involvement of a catecholamine-mediated bacterial signaling axis in colitis pathogenesis. Enterobacteriaceae sense and respond to microbiota-generated signals and host-derived catecholamines through the two-component quorum-sensing Escherichia coli regulators B and C (QseBC) system. On signal detection, QseC activates a cascade to induce virulence gene expression. Although a single pathogen has not been identified as a causative agent in IBD, adherent-invasive Escherichia coli (AIEC) have been implicated. Flagellar expression is necessary for the IBD-associated AIEC strain LF82 to establish colonization. Thus, we hypothesized that qseC inactivation could reduce LF82's virulence, and found that an absence of qseC leads to down-regulated flagellar expression and motility in vitro and reduced colonization in vivo. We extend these findings on the potential of QseC-based IBD therapeutics to three preclinical IBD models, wherein we observe that QseC blockade can effectively modulate colitogenic microbiotas to reduce intestinal inflammation. Collectively, our data support a role for QseC-mediated bacterial signaling in IBD pathogenesis and indicate that QseC inhibition may be a useful microbiota-targeted approach for disease management.colitis | Escherichia coli | QseC | antivirulence | gut microbiome

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Section: Resultssupporting

confidence: 71%

Section: Resultsmentioning

confidence: 99%

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QseC inhibition as an antivirulence approach for colitis-associated bacteria

Rooks

Veiga

Reeves

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Additionally, a single oral dose of LED209 afforded protection to mice that were preexposed to Francisella tularensis, another pathogen in which AI-3-based QS contributes to virulence (188). Unfortunately, although LED209 did not inhibit EHEC growth (188), a recent study found that deletion of qseC results in large metabolic changes in both F. tularensis and EHEC that consequently affect virulence factor production (227). Thus, QseC inhibition is likely both an antimicrobial and an anti-QS strategy.…”

Section: Inhibition Of Signal Detection Synthetic Signal Analogues Anmentioning

confidence: 99%

Exploiting Quorum Sensing To Confuse Bacterial Pathogens

LaSarre

Federle

2013

Microbiol Mol Biol Rev

690

556

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SUMMARY Cell-cell communication, or quorum sensing, is a widespread phenomenon in bacteria that is used to coordinate gene expression among local populations. Its use by bacterial pathogens to regulate genes that promote invasion, defense, and spread has been particularly well documented. With the ongoing emergence of antibiotic-resistant pathogens, there is a current need for development of alternative therapeutic strategies. An antivirulence approach by which quorum sensing is impeded has caught on as a viable means to manipulate bacterial processes, especially pathogenic traits that are harmful to human and animal health and agricultural productivity. The identification and development of chemical compounds and enzymes that facilitate quorum-sensing inhibition (QSI) by targeting signaling molecules, signal biogenesis, or signal detection are reviewed here. Overall, the evidence suggests that QSI therapy may be efficacious against some, but not necessarily all, bacterial pathogens, and several failures and ongoing concerns that may steer future studies in productive directions are discussed. Nevertheless, various QSI successes have rightfully perpetuated excitement surrounding new potential therapies, and this review highlights promising QSI leads in disrupting pathogenesis in both plants and animals.

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“…8 UPEC harbor numerous CUP pili systems, the differential expression of which is thought to facilitate colonization of different niches. [9][10][11][12][13] Type 1 pili mediate adherence largely via the FimH tip adhesin, which recognizes and binds mannosylated moieties on biotic and abiotic surfaces. 4,6,[14][15][16][17][18][19][20] Within the host, FimH mediates UPEC binding to the bladder epithelium and is also required for proper formation of biofilm-like intracellular bacterial communities (IBCs) within bladder epithelial cells.…”

mentioning

confidence: 99%