Imperial College London

DrAndrewEdwards

Faculty of MedicineDepartment of Medicine

Non-Clinical Lecturer in Molecular Microbiology
 
 
 
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Contact

 

a.edwards Website

 
 
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Location

 

5.40AFlowers buildingSouth Kensington Campus

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Summary

 

Publications

Publication Type
Year
to

26 results found

Painter KL, Hall A, Ha KP, Edwards Aet al., The electron transport chain sensitisesStaphylococcus aureus and Enterococcus faecalis to the oxidative burst, Infection and Immunity, ISSN: 0019-9567

JOURNAL ARTICLE

Ledger EVK, Pader V, Edwards AM, 2017, Enterococcus faecalis and pathogenic streptococci inactivate daptomycin by releasing phospholipids, Microbiology, ISSN: 1350-0872

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Pader V, Edwards AM, 2017, Daptomycin: new insights into an antibiotic of last resort, FUTURE MICROBIOLOGY, Vol: 12, Pages: 461-464, ISSN: 1746-0913

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Pader V, Hakim S, Painter KL, Wigneshweraraj S, Clarke TB, Edwards AMet al., 2017, Staphylococcus aureus inactivates daptomycin by releasing membrane phospholipids, NATURE MICROBIOLOGY, Vol: 2, ISSN: 2058-5276

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Painter KL, Strange E, Parkhill J, Bamford KB, Armstrong-James D, Edwards AMet al., 2015, Staphylococcus aureus Adapts to Oxidative Stress by Producing H2O2-Resistant Small-Colony Variants via the SOS Response, INFECTION AND IMMUNITY, Vol: 83, Pages: 1830-1844, ISSN: 0019-9567

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Pader V, James EH, Painter KL, Wigneshweraraj S, Edwards AMet al., 2014, The Agr Quorum-Sensing System Regulates Fibronectin Binding but Not Hemolysis in the Absence of a Functional Electron Transport Chain, INFECTION AND IMMUNITY, Vol: 82, Pages: 4337-4347, ISSN: 0019-9567

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Painter KL, Krishna A, Wigneshweraraj S, Edwards AMet al., 2014, What role does the quorum-sensing accessory gene regulator system play during Staphylococcus aureus bacteremia?, TRENDS IN MICROBIOLOGY, Vol: 22, Pages: 676-685, ISSN: 0966-842X

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Rudkin JK, Laabei M, Edwards AM, Joo H-S, Otto M, Lennon KL, O'Gara JP, Waterfield NR, Massey RCet al., 2014, Oxacillin Alters the Toxin Expression Profile of Community-Associated Methicillin-Resistant Staphylococcus aureus, ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, Vol: 58, Pages: 1100-1107, ISSN: 0066-4804

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Stemberk V, Jones RPO, Moroz O, Atkin KE, Edwards AM, Turkenburg JP, Leech AP, Massey RC, Potts JRet al., 2014, Evidence for Steric Regulation of Fibrinogen Binding to Staphylococcus aureus Fibronectin-binding Protein A ( FnBPA), JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 289, Pages: 12842-12851, ISSN: 0021-9258

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James EH, Edwards AM, Wigneshweraraj S, 2013, Transcriptional downregulation of agr expression in Staphylococcus aureus during growth in human serum can be overcome by constitutively active mutant forms of the sensor kinase AgrC, FEMS MICROBIOLOGY LETTERS, Vol: 349, Pages: 153-162, ISSN: 0378-1097

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Edwards AM, 2012, Phenotype-switching is a natural consequence of Staphylococcus aureus replication, Journal of Bacteriology

The pathogen Staphylococcus aureus undergoes phenotype-switching in vivo from its normal colony phenotype (NCP) to a slow-growing, antibiotic-resistant small colony variant (SCV) phenotype, which is associated with persistence in host cells and tissues. However, it is not clear whether phenotype-switching is the result of a constitutive process that is selected for under certain conditions, or is triggered by particular environmental stimuli. Examination of cultures of diverse S. aureus strains in the absence of selective pressure consistently revealed a small gentamicin-resistant SCV sub-population, which emerged during exponential-phase NCP growth and increased in number until NCP stationary phase. Treatment of replicating bacteria with the antibiotic gentamicin, which inhibited NCP but not SCV replication, resulted in an initial decrease in SCV numbers, demonstrating that SCVs arise as a consequence of NCP replication. However, SCV population expansion in the presence of gentamicin was re-established by selection of phenotype-stable SCVs and subsequent SCV replication. In the absence of selective pressure however, phenotype-switching was bi-directional and occurred at a high frequency during NCP replication, resulting in SCV turnover. In summary, these data demonstrate that S. aureus phenotype-switching occurs via a constitutive mechanism that generates a dynamic, antibiotic-resistant sub-population of bacteria that can revert to the parental phenotype. The emergence of SCVs can therefore be considered a normal part of the S. aureus life-cycle and provides an insurance policy against exposure to antibiotics that would otherwise eliminate the entire population.

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Edwards AM, Bowden MG, Brown EL, Laabei M, Massey RCet al., 2012, Staphylococcus aureus Extracellular Adherence Protein triggers TNFα release, promoting attachment to endothelial cells via protein A., Plos One, Vol: (8)

Staphylococcus aureus is a leading cause of bacteraemia, which frequently results in complications such as infective endocarditis, osteomyelitis and exit from the bloodstream to cause metastatic abscesses. Interaction with endothelial cells is critical to these complications and several bacterial proteins have been shown to be involved. The S. aureus extracellular adhesion protein (Eap) has many functions, it binds several host glyco-proteins and has both pro- and anti-inflammatory activity. Unfortunately its role in vivo has not been robustly tested to date, due to difficulties in complementing its activity in mutant strains. We previously found Eap to have pro-inflammatory activity, and here show that purified native Eap triggered TNFα release in whole human blood in a dose-dependent manner. This level of TNFα increased adhesion of S. aureus to endothelial cells 4-fold via a mechanism involving protein A on the bacterial surface and gC1qR/p33 on the endothelial cell surface. The contribution this and other Eap activities play in disease severity during bacteraemia was tested by constructing an isogenic set of strains in which the eap gene was inactivated and complemented by inserting an intact copy elsewhere on the bacterial chromosome. Using a murine bacteraemia model we found that Eap expressing strains cause a more severe infection, demonstrating its role in invasive disease.

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Edwards AM, Massey RC, Clarke SR, 2012, Molecular mechanisms of Staphylococcus aureus nasopharyngeal colonization, MOLECULAR ORAL MICROBIOLOGY, Vol: 27, Pages: 1-10, ISSN: 2041-1006

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Rudkin JK, Edwards AM, Bowden MG, Brown EL, Pozzi C, Waters EM, Chan WC, Williams P, O'Gara JP, Massey RCet al., 2012, Methicillin Resistance Reduces the Virulence of Healthcare-Associated Methicillin-Resistant Staphylococcus aureus by Interfering With the agr Quorum Sensing System, JOURNAL OF INFECTIOUS DISEASES, Vol: 205, Pages: 798-806, ISSN: 0022-1899

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Edwards AM, Massey RC, 2011, How does Staphylococcus aureus escape the bloodstream?, TRENDS IN MICROBIOLOGY, Vol: 19, Pages: 184-190, ISSN: 0966-842X

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Edwards AM, Massey RC, 2011, Invasion of Human Cells by a Bacterial Pathogen, JOVE-JOURNAL OF VISUALIZED EXPERIMENTS, ISSN: 1940-087X

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Edwards AM, Potter U, Meenan NAG, Potts JR, Massey RCet al., 2011, Staphylococcus aureus Keratinocyte Invasion Is Dependent upon Multiple High-Affinity Fibronectin-Binding Repeats within FnBPA, PLOS ONE, Vol: 6, ISSN: 1932-6203

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Edwards AM, Potts JR, Josefsson E, Massey RCet al., 2010, Staphylococcus aureus Host Cell Invasion and Virulence in Sepsis Is Facilitated by the Multiple Repeats within FnBPA, PLOS PATHOGENS, Vol: 6, ISSN: 1553-7366

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Edwards AM, Manetti AGO, Falugi F, Zingaretti C, Capo S, Buccato S, Bensi G, Telford JL, Margarit I, Grandi Get al., 2008, Scavenger receptor gp340 aggregates group A streptococci by binding pili, MOLECULAR MICROBIOLOGY, Vol: 68, Pages: 1378-1394, ISSN: 0950-382X

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Edwards AM, Grossman TJ, Rudney JD, 2007, Association of a high-molecular weight arginine-binding protein of Fusobacterium nucleatum ATCC 10953 with adhesion to secretory immunoglobulin A and coaggregation with Streptococcus cristatus, ORAL MICROBIOLOGY AND IMMUNOLOGY, Vol: 22, Pages: 217-224, ISSN: 0902-0055

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Manetti AGO, Zingaretti C, Falugi F, Capo S, Bombaci M, Bagnoli F, Gambellini G, Bensi G, Mora M, Edwards AM, Musser JM, Graviss EA, Telford JL, Grandi G, Margarit Iet al., 2007, Streptococcus pyogenes pili promote pharyngeal cell adhesion and biofilm formation, MOLECULAR MICROBIOLOGY, Vol: 64, Pages: 968-983, ISSN: 0950-382X

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Edwards AM, Grossman TJ, Rudney JD, 2006, Fusobacterium nucleatum transports noninvasive Streptococcus cristatus into human epithelial cells, INFECTION AND IMMUNITY, Vol: 74, Pages: 654-662, ISSN: 0019-9567

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Edwards AM, Jenkinson HF, Woodward MJ, Dymock Det al., 2005, Binding properties and adhesion-mediating regions of the major sheath protein of Treponema denticola ATCC 35405, INFECTION AND IMMUNITY, Vol: 73, Pages: 2891-2898, ISSN: 0019-9567

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Hill DJ, Edwards AM, Rowe HA, Virji Met al., 2005, Carcinoembryonic antigen-related cell adhesion molecule (CEACAM)-binding recombinant polypeptide confers protection against infection by respiratory and urogenital pathogens, MOLECULAR MICROBIOLOGY, Vol: 55, Pages: 1515-1527, ISSN: 0950-382X

JOURNAL ARTICLE

Edwards AM, Dymock D, Jenkinson HF, 2003, From tooth to hoof: treponemes in tissue-destructive diseases, J.Appl.Microbiol., Vol: 94, Pages: 767-780

With the advent of new molecular and immunological tools, there is better understanding of the roles that difficult to cultivate bacteria, and not-yet-cultivated bacteria such as spirochaetes, play in polymicrobial diseases. Only relatively recently have studies implicated Treponema spirochaetes in human periodontal disease, a destructive condition of the tissues supporting the teeth. A number of different Treponema species have been isolated and their surface protein components that mediate adhesion, cytotoxicity, and tissue damage have been characterized. More recently Treponema strains closely related to human oral isolates have been cultivated from active lesions of digital dermatitis, an ulcerative condition affecting the feet of cows and sheep. This condition, like periodontal disease, appears to have a polymicrobial aetiology in which enrichment for Treponema may play a crucial part. This article reviews the known mechanisms by which Treponema interact with eukaryotic host cells and tissue proteins, and how these interactions may contribute to pathogenic diversity

JOURNAL ARTICLE

Edwards AM, Dymock D, Woodward MJ, Jenkinson HFet al., 2003, Genetic relatedness and phenotypic characteristics of Treponema associated with human periodontal tissues and ruminant foot disease, Microbiology, Vol: 149, Pages: 1083-1093

Treponema have been implicated recently in the pathogenesis of digital dermatitis (DD) and contagious ovine digital dermatitis (CODD) that are infectious diseases of bovine and ovine foot tissues, respectively. Previous analyses of treponemal 16S rDNA sequences, PCR-amplified directly from DD or CODD lesions, have suggested relatedness of animal Treponema to some human oral Treponema species isolated from periodontal tissues. In this study a range of adhesion and virulence-related properties of three animal Treponema isolates have been compared with representative human oral strains of Treponema denticola and Treponema vincentii. In adhesion assays using biotinylated treponemal cells, T. denticola cells bound in consistently higher numbers to fibronectin, laminin, collagen type I, gelatin, keratin and lactoferrin than did T. vincentii or animal Treponema isolates. However, animal DD strains adhered to fibrinogen at equivalent or greater levels than T. denticola. All Treponema strains bound to the amino-terminal heparin I/fibrin I domain of fibronectin. 16S rDNA sequence analyses placed ovine strain UB1090 and bovine strain UB1467 within a cluster that was phylogenetically related to T. vincentii, while ovine strain UB1466 appeared more closely related to T. denticola. These observations correlated with phenotypic properties. Thus, T. denticola ATCC 35405, GM-1, and Treponema UB1466 had similar outer-membrane protein profiles, produced chymotrypsin-like protease (CTLP), trypsin-like protease and high levels of proline iminopeptidase, and co-aggregated with human oral bacteria Porphyromonas gingivalis and Streptococcus crista. Conversely, T. vincentii ATCC 35580, D2A-2, and animal strains UB1090 and UB1467 did not express CTLP or trypsin-like protease and did not co-aggregate with P. gingivalis or S. crista. Taken collectively, these results suggest that human oral-related Treponema have broad host specificity and that similar control or preventive strategies might be

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