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• Journal article
  Williams TJ, Harvey S, Armstrong-James D, 2020,

  Immunotherapeutic approaches for fungal infections

  , CURRENT OPINION IN MICROBIOLOGY, Vol: 58, Pages: 130-137, ISSN: 1369-5274
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  • Citations: 10
• Journal article
  Murray A, Cass L, Ito K, Pagani N, Armstrong-James D, Dalal P, Reed A, Strong Pet al., 2020,

  PC945, a Novel Inhaled Antifungal Agent, for the Treatment of Respiratory Fungal Infections

  , JOURNAL OF FUNGI, Vol: 6
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  • Citations: 13
• Journal article
  Zhyvoloup A, Yu BYK, Bakovic J, Davis-Lunn M, Tossounian M-A, Thomas N, Tsuchiya Y, Peak-Chew SY, Wigneshweraraj S, Filonenko V, Skehel M, Setlow P, Gout Iet al., 2020,

  Analysis of disulphide bond linkage between CoA and protein cysteine thiols during sporulation and in spores of <i>Bacillus</i> species

  , FEMS MICROBIOLOGY LETTERS, Vol: 367, ISSN: 0378-1097
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  • Citations: 5
• Journal article
  Sweeney E, Sabnis A, Edwards AM, Harrison Fet al., 2020,

  Effect of host-mimicking medium and biofilm growth on the ability of colistin to kill Pseudomonas aeruginosa

  , MICROBIOLOGY-SGM, Vol: 166, Pages: 1171-1180, ISSN: 1350-0872

  In vivo biofilms cause recalcitrant infections with extensive and unpredictable antibiotic tolerance. Here, we demonstrate increased tolerance of colistin by Pseudomonas aeruginosa when grown in medium that mimics cystic fibrosis (CF) sputum versus standard medium in in vitro biofilm assays, and drastically increased tolerance when grown in an ex vivo CF model versus the in vitro assay. We used colistin conjugated to the fluorescent dye BODIPY to assess the penetration of the antibiotic into ex vivo biofilms and showed that poor penetration partly explains the high doses of drug necessary to kill bacteria in these biofilms. The ability of antibiotics to penetrate the biofilm matrix is key to their clinical success, but hard to measure. Our results demonstrate both the importance of reduced entry into the matrix in in vivo-like biofilm, and the tractability of using a fluorescent tag and benchtop fluorimeter to assess antibiotic entry into biofilms. This method could be a relatively quick, cheap and useful addition to diagnostic and drug development pipelines, allowing the assessment of drug entry into biofilms, in in vivo-like conditions, prior to more detailed tests of biofilm killing.

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• Journal article
  Saromi K, England P, Tang W, Kostrzewa M, Corran A, Woscholski R, Larrouy-Maumus Get al., 2020,

  Rapid glycosyl-inositol-phospho-ceramide fingerprint from filamentous fungal pathogens using the MALDI Biotyper Sirius system

  , RAPID COMMUNICATIONS IN MASS SPECTROMETRY, Vol: 34, ISSN: 0951-4198
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  • Citations: 3
• Journal article
  Lin H-H, Filloux A, Lai E-M, 2020,

  Role of recipient susceptibility factors during contact-dependent interbacterial competition

  , Frontiers in Microbiology, Vol: 11, Pages: 1-15, ISSN: 1664-302X

  Bacteria evolved multiple strategies to survive and develop optimal fitness in their ecological niche. They deployed protein secretion systems for robust and efficient delivery of antibacterial toxins into their target cells, therefore inhibiting their growth or killing them. To maximize antagonism, recipient factors on target cells can be recognized or hijacked to enhance the entry or toxicity of these toxins. To date, knowledge regarding recipient susceptibility (RS) factors and their mode of action is mostly originating from studies on the type Vb secretion system that is also known as the contact-dependent inhibition (CDI) system. Yet, recent studies on the type VI secretion system (T6SS), and the CDI by glycine-zipper protein (Cdz) system, also reported the emerging roles of RS factors in interbacterial competition. Here, we review these RS factors and their mechanistic impact in increasing susceptibility of recipient cells in response to CDI, T6SS, and Cdz. Past and future strategies for identifying novel RS factors are also discussed, which will help in understanding the interplay between attacker and prey upon secretion system-dependent competition. Understanding these mechanisms would also provide insights for developing novel antibacterial strategies to antagonize aggressive bacteria-killing pathogens.

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• Journal article
  Yong HY, Larrouy-Maumus G, Zloh M, Smyth R, Ataya R, Benton CM, Munday MRet al., 2020,

  Early detection of metabolic changes in drug-induced steatosis using metabolomics approaches

  , RSC ADVANCES, Vol: 10, Pages: 41047-41057
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  • Citations: 3
• Conference paper
  Miguens Blanco J, Selvarajah U, Liu Z, Mullish BH, Alexander J, McDonald J, Abraham S, Marchesi Jet al., 2020,

  Identification of New Associations Between Psoriatic Arthritis and the Gut Microbiota. the Mi-PART, a Phenomic Study

  , ACR Convergence 2020, Publisher: Wiley, ISSN: 2326-5205
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• Journal article
  Martinez-Gili L, McDonald JAK, Liu Z, Kao D, Allegretti JR, Monaghan TM, Barker GF, Miguéns Blanco J, Williams HRT, Holmes E, Thursz MR, Marchesi JR, Mullish BHet al., 2020,

  Understanding the mechanisms of efficacy of fecal microbiota transplant in treating recurrent <i>Clostridioides difficile</i> infection and beyond: the contribution of gut microbial-derived metabolites

  , Gut Microbes, Vol: 12, Pages: 1810531-1810531, ISSN: 1949-0976
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• Journal article
  Ranganathan N, Johnson R, Edwards AM, 2020,

  The general stress response of Staphylococcus aureus promotes tolerance of antibiotics and survival in whole human blood

  , MICROBIOLOGY-SGM, Vol: 166, Pages: 1088-1094, ISSN: 1350-0872

  Staphylococcus aureus is a frequent cause of invasive human infections such as bacteraemia and infective endocarditis. These infections frequently relapse or become chronic, suggesting that the pathogen has mechanisms to tolerate the twin threats of therapeutic antibiotics and host immunity. The general stress response of S. aureus is regulated by the alternative sigma factor B (σB) and provides protection from multiple stresses including oxidative, acidic and heat. σB also contributes to virulence, intracellular persistence and chronic infection. However, the protective effect of σB on bacterial survival during exposure to antibiotics or host immune defences is poorly characterized. We found that σB promotes the survival of S. aureus exposed to the antibiotics gentamicin, ciprofloxacin, vancomycin and daptomycin, but not oxacillin or clindamycin. We also found that σB promoted staphylococcal survival in whole human blood, most likely via its contribution to oxidative stress resistance. Therefore, we conclude that the general stress response of S. aureus may contribute to the development of chronic infection by conferring tolerance to both antibiotics and host immune defences.

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