FNR Regulates Expression of Important Virulence Factors Contributing to Pathogenicity of Uropathogenic Escherichia coli

Barbieri, Nicolle Lima; Nicholson, Bryon A.; Hussein, Hussein Awad; Cai, Wentong; Wannemuehler, Yvonne; Dell'Anna, Giuseppe; Logue, Catherine M.; Horn, Fabiana; Nolan, Lisa K.; Li, Ganwu

doi:10.1128/iai.02315-14

Cited by 46 publications

(57 citation statements)

References 49 publications

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“…Indirectly, in a rfaH strain, secretion of HlyA is impaired as TolC insertion in the outer membrane in misregulated (27) . Another global regulator of E. coli, fumarate and nitrate reduction (FNR), modulates hemolysin expression under anaerobic conditions in vitro, similar to conditions that are likely to be encountered in vivo (28) . The importance of this regulator was assessed in the CFT073 background.…”

Section: Accepted Manuscriptmentioning

confidence: 98%

Hemolysin of uropathogenic Escherichia coli: A cloak or a dagger?

Ristow¹,

Welch²

2016

Biochimica et Biophysica Acta (BBA) - Biomembranes

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Hemolysin from uropathogenic Escherichia coli (UPEC) is a hemolytic and cytotoxic protein active against a broad range of species and cell types. Expression of hemolysin correlates with severity of infection, as up to 78% of UPEC isolates from pyelonephritis cases express hemolysin. Despite decades of research on hemolysin activity, the mechanism of intoxication and the function of hemolysin in UPEC infection remain elusive. Early in vitro research established the role of hemolysin as a lytic protein at high doses. It is hypothesized that hemolysin is secreted at sublytic doses in vivo and recent research has focused on understanding the more subtle effects of hemolysin both in vitro and in elegant infection models in vivo, including inoculation by micropuncture of individual kidney nephrons. As the field continues to evolve, comparisons of hemolysin function in isolates from a range of UTI infections will be important for delineating the role of this toxin. This article is part of a Special Issue entitled: Pore-Forming Toxins edited by Mauro Dalla Serra and Franco Gambale.

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Section: Accepted Manuscriptmentioning

confidence: 98%

Hemolysin of uropathogenic Escherichia coli: A cloak or a dagger?

Ristow¹,

Welch²

2016

Biochimica et Biophysica Acta (BBA) - Biomembranes

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“…which cause host uroepithelial injury, cell lysis, and the subsequent release of intra-cellular micronutrients (36)(37)(38).…”

Section: Urinary Tract Infection-associated Vfsmentioning

confidence: 99%

Extra-intestinal pathogenic Escherichia coli (ExPEC): Disease, carriage and clones

Dale

Woodford

2015

Journal of Infection

165

132

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Extra-intestinal pathogenic E. coli (ExPEC) have a complex phylogeny, broad virulence factor (VF) armament and significant genomic plasticity, and are associated with a spectrum of host infective syndromes ranging from simple urinary tract infection to life-threatening bacteraemia. Their importance as pathogens has come to the fore in recent years, particularly in the context of the global emergence of hyper-virulent and antibiotic resistant strains.Despite this, the mechanisms underlying ExPEC transmission dynamics and clonal selection remain poorly understood. Large-scale epidemiological and clinical studies are urgently required to ascertain the mechanisms underlying these processes to enable the development of novel evidence-based preventative and therapeutic strategies. In the current review, we provide a concise summary of the methods utilised for ExPEC phylogenetic genetic delineation before exploring in detail the associations between ExPEC VFs and site-specific disease. We then consider the role of ExPEC as an intestinal colonist before outlining known associations between ExPEC clonal variation, specific disease syndromes and antibiotic resistance.

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“…To verify that this impact on mortality was not due to an unwanted mutation, a stable low-copy-number plasmid, pGEN-MCS, which had been successfully used for an in vivo complementation assay (10,16,17), was used to construct a mutant complementation strain. To do this, the coding region of arcA plus its predicted promoter region was cloned into pGEN-MCS, and the resultant plasmid was transformed into the arcA mutant.…”

Section: Resultsmentioning

confidence: 99%

“…This contrasts to the targets of FNR, another factor that mediates bacterial adaptation to anaerobic conditions. Studies of uropathogenic E. coli (UPEC) indicate that FNR regulates genes controlling motility and multiple virulence factors (including expression of type I and P fimbriae), modulation of hemolysin expression, and expression of a novel pathogenicity island involved in ␣-ketoglutarate metabolism (10). This may or may not be due to the facts that (i) the FNR study targeted UPEC strain CFT073 (serotype O6:K2:H1), a distinct clade within B2 strains, and (ii) the conditions used for transcriptome examinations differed.…”

Section: Figmentioning

confidence: 99%

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ArcA Controls Metabolism, Chemotaxis, and Motility Contributing to the Pathogenicity of Avian Pathogenic Escherichia coli

Jiang

Bao

et al. 2015

Infect Immun

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f Avian pathogenic Escherichia coli (APEC) strains cause one of the three most significant infectious diseases in the poultry industry and are also potential food-borne pathogens threating human health. In this study, we showed that ArcA (aerobic respiratory control), a global regulator important for E. coli's adaptation from anaerobic to aerobic conditions and control of that bacterium's enzymatic defenses against reactive oxygen species (ROS), is involved in the virulence of APEC. Deletion of arcA significantly attenuates the virulence of APEC in the duck model. Transcriptome sequencing (RNA-Seq) analyses comparing the APEC wild type and the arcA mutant indicate that ArcA regulates the expression of 129 genes, including genes involved in citrate transport and metabolism, flagellum synthesis, and chemotaxis. Further investigations revealed that citCEFXG contributed to APEC's microaerobic growth at the lag and log phases when cultured in duck serum and that ArcA played a dual role in the control of citrate metabolism and transportation. In addition, deletion of flagellar genes motA and motB and chemotaxis gene cheA significantly attenuated the virulence of APEC, and ArcA was shown to directly regulate the expression of motA, motB, and cheA. The combined results indicate that ArcA controls metabolism, chemotaxis, and motility contributing to the pathogenicity of APEC. Commensal and pathogenic Escherichia coli strains can grow under both aerobic and anaerobic conditions. The enzymes required for catabolism under aerobic versus anaerobic conditions are substantially different, and E. coli has the ability to switch among anaerobic, anaerobic respiratory, and fermentative pathways (1). The expression of genes involved in cellular functions such as nutrient uptake and/or excretion systems, biosynthetic pathways, and macromolecular synthesis are also adjusted in response to oxygen availability (2). The Arc two-component signal transduction system, comprised of the kinase sensor ArcB and its cognate response regulator ArcA, is one of the mechanisms that enable E. coli adaptation to changing oxygen availability (3). Once an environmental signal is received, ArcB undergoes autophosphorylation and catalyzes the transphosphorylation of ArcA, which then promotes or represses expression of Arc-regulated genes. Rather than directly detecting environmental O 2 , ArcB probably senses the redox state of the cell through detection of a reduced electron transport component (4). Under aerobic conditions (5), oxidized forms of quinone electron carriers in the membrane inhibit the autophosphorylation of ArcB, while under anaerobic and microaerobic conditions, ArcB undergoes autophosphorylation. The net activity of ArcB as a kinase for ArcA is expected to progressively increase during the transition from aerobic to anaerobic growth.The ArcA regulon of E. coli K-12 strains has been extensively studied under both aerobic and anaerobic conditions (6, 7). A previous study indicated that about 1,139 genes in the E. coli K-12 genome are regu...

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FNR Regulates Expression of Important Virulence Factors Contributing to Pathogenicity of Uropathogenic Escherichia coli

Cited by 46 publications

References 49 publications

Hemolysin of uropathogenic Escherichia coli: A cloak or a dagger?

Hemolysin of uropathogenic Escherichia coli: A cloak or a dagger?

Extra-intestinal pathogenic Escherichia coli (ExPEC): Disease, carriage and clones

ArcA Controls Metabolism, Chemotaxis, and Motility Contributing to the Pathogenicity of Avian Pathogenic Escherichia coli

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