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• Journal article
  Sidhu JK, Siggins MK, Liew F, Russell CD, Uruchurtu ASS, Davis C, Turtle L, Moore SC, Hardwick HE, Oosthuyzen W, Thomson EC, Semple MG, Baillie JK, Openshaw PJM, Thwaites RS, ISARIC4C investigatorset al., 2024,

  Delayed mucosal antiviral responses despite robust peripheral inflammation in fatal COVID-19

  , Journal of Infectious Diseases, Vol: 230, Pages: e17-e29, ISSN: 0022-1899

  BackgroundWhile inflammatory and immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in peripheral blood are extensively described, responses at the upper respiratory mucosal site of initial infection are relatively poorly defined. We sought to identify mucosal cytokine/chemokine signatures that distinguished coronavirus disease 2019 (COVID-19) severity categories, and relate these to disease progression and peripheral inflammation.MethodsWe measured 35 cytokines and chemokines in nasal samples from 274 patients hospitalized with COVID-19. Analysis considered the timing of sampling during disease, as either the early (0–5 days after symptom onset) or late (6–20 days after symptom onset) phase.ResultsPatients that survived severe COVID-19 showed interferon (IFN)-dominated mucosal immune responses (IFN-γ, CXCL10, and CXCL13) early in infection. These early mucosal responses were absent in patients who would progress to fatal disease despite equivalent SARS-CoV-2 viral load. Mucosal inflammation in later disease was dominated by interleukin 2 (IL-2), IL-10, IFN-γ, and IL-12p70, which scaled with severity but did not differentiate patients who would survive or succumb to disease. Cytokines and chemokines in the mucosa showed distinctions from responses evident in the peripheral blood, particularly during fatal disease.ConclusionsDefective early mucosal antiviral responses anticipate fatal COVID-19 but are not associated with viral load. Early mucosal immune responses may define the trajectory of severe COVID-19.

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• Journal article
  Davies J, Mossop M, Jonathan I-H, Hughes D, Dobra R, Cunanan A, Rosenthal M, Carr S, Ramadan N, Nolan Let al., 2024,

  Chronicity counts: the impact of P. aeruginosa, S. aureus, and co-infection in cystic fibrosis

  , American Journal of Respiratory and Critical Care Medicine, Vol: 210, Pages: 240-242, ISSN: 1073-449X
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• Journal article
  Thwaites R, Sidhu J, Siggins M, Liew F, Russel C, Uruchurtu A, Davis C, Turtle L, Moore S, Hardwick H, Oosthuyzen W, Thomson E, Semple M, Baillie JK, Openshaw Pet al., 2024,

  Delayed mucosal anti-viral responses despite robust peripheral inflammation in fatal COVID-19

  , Journal of Infectious Diseases, Vol: 230, Pages: e17-e29, ISSN: 0022-1899

  Background:While inflammatory and immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in peripheral blood are extensively described, responses at the upper respiratory mucosal site of initial infection are relatively poorly defined. We sought to identify mucosal cytokine/chemokine signatures that distinguished coronavirus disease 2019 (COVID-19) severity categories, and relate these to disease progression and peripheral inflammation.Methods:We measured 35 cytokines and chemokines in nasal samples from 274 patients hospitalized with COVID-19. Analysis considered the timing of sampling during disease, as either the early (0–5 days after symptom onset) or late (6–20 days after symptom onset) phase.Results:Patients that survived severe COVID-19 showed interferon (IFN)-dominated mucosal immune responses (IFN-γ, CXCL10, and CXCL13) early in infection. These early mucosal responses were absent in patients who would progress to fatal disease despite equivalent SARS-CoV-2 viral load. Mucosal inflammation in later disease was dominated by interleukin 2 (IL-2), IL-10, IFN-γ, and IL-12p70, which scaled with severity but did not differentiate patients who would survive or succumb to disease. Cytokines and chemokines in the mucosa showed distinctions from responses evident in the peripheral blood, particularly during fatal disease.Conclusions:Defective early mucosal antiviral responses anticipate fatal COVID-19 but are not associated with viral load. Early mucosal immune responses may define the trajectory of severe COVID-19.

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• Journal article
  Mall MA, Davies JC, Donaldson SH, Jain R, Chalmers JD, Shteinberg Met al., 2024,

  Neutrophil serine proteases in cystic fibrosis: role in disease pathogenesis and rationale as a therapeutic target

  , European Respiratory Review, Vol: 33, ISSN: 0905-9180

  Chronic airway inflammation is a central feature in the pathogenesis of bronchiectasis (BE), which can be caused by cystic fibrosis (CFBE; hereafter referred to as CF lung disease) and non-CF-related conditions (NCFBE). Inflammation in both CF lung disease and NCFBE is predominantly driven by neutrophils, which release proinflammatory cytokines and granule proteins, including neutrophil serine proteases (NSPs). NSPs include neutrophil elastase, proteinase 3 and cathepsin G. An imbalance between NSPs and their antiproteases has been observed in people with CF lung disease and people with NCFBE. While the role of the protease/antiprotease imbalance is well established in both CF lung disease and NCFBE, effective therapies targeting NSPs are lacking. In recent years, the introduction of CF transmembrane conductance regulator (CFTR) modulator therapy has immensely improved outcomes in many people with CF (pwCF). Despite this, evidence suggests that airway inflammation persists, even in pwCF treated with CFTR modulator therapy. In this review, we summarise current data on neutrophilic inflammation in CF lung disease to assess whether neutrophilic inflammation and high, uncontrolled NSP levels play similar roles in CF lung disease and in NCFBE. We discuss similarities between the neutrophilic inflammatory profiles of people with CF lung disease and NCFBE, potentially supporting a similar therapeutic approach. Additionally, we present evidence suggesting that neutrophilic inflammation persists in pwCF treated with CFTR modulator therapy, at levels similar to those in people with NCFBE. Collectively, these findings highlight the ongoing need for new treatment strategies targeting neutrophilic inflammation in CF lung disease.

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• Journal article
  Leavy OC, Russell RJ, Harrison EM, Lone NI, Kerr S, Docherty AB, Sheikh A, Richardson M, Elneima O, Greening NJ, Harris VC, Houchen-Wolloff L, McAuley HJC, Saunders RM, Sereno M, Shikotra A, Singapuri A, Aul R, Beirne P, Bolton CE, Brown JS, Choudhury G, Bakerly ND, Easom N, Echevarria C, Fuld J, Hart N, Hurst JR, Jones M, Parekh D, Pfeffer P, Rahman NM, Rowland-Jones S, Shah AM, Wootton DG, Jolley C, Thompson AAR, Chalder T, Davies MJ, De Soyza A, Geddes JR, Greenhalf W, Heller S, Howard L, Jacob J, Jenkins RG, Lord JM, Man WD-C, McCann GP, Neubauer S, Openshaw PJM, Porter J, Rowland MJ, Scott JT, Semple MG, Singh SJ, Thomas D, Toshner M, Lewis K, Heaney LG, Briggs A, Zheng B, Thorpe M, Quint JK, Chalmers JD, Ho L-P, Horsley A, Marks M, Poinasamy K, Raman B, Wain LV, Brightling CE, Evans RAet al., 2024,

  1-year health outcomes associated with systemic corticosteroids for COVID-19: a longitudinal cohort study

  , ERJ OPEN RESEARCH, Vol: 10
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• Journal article
  Sintoris S, Binkowska JM, Gillan JL, Zuurbier RP, Twynam-Perkins J, Kristensen M, Melrose L, Parga PL, Rodriguez AR, Chu ML, van Boeckel SR, Wildenbeest JG, Bowdish DME, Currie AJ, Thwaites RS, Schwarze J, van Houten MA, Boardman JP, Cunningham S, Bogaert D, Davidson DJet al., 2024,

  Nasal cathelicidin is expressed in early life and is increased during mild, but not severe respiratory syncytial virus infection

  , SCIENTIFIC REPORTS, Vol: 14, ISSN: 2045-2322
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• Journal article
  Tung NWH, Edmondson C, Westrupp N, Rosenthal M, Davies JCet al., 2024,

  Neutrophil-to-lymphocyte ratio as a biomarker of acute pulmonary exacerbations in children with cystic fibrosis: a retrospective cohort study

  , ARCHIVES OF DISEASE IN CHILDHOOD, ISSN: 0003-9888
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• Journal article
  Matthews J, Dobra R, Wilson G, Allen L, Bossley C, Brendell R, Brugha R, Brown D, Brown S, Cadiente S, Cameron L, Davies G, Dawson C, Elborn S, Hughes D, Longmate J, Macedo P, Pappas L, Pao C, Round C, Ruiz G, Saunders C, Shafi N, Simmonds N, Waller M, Watson D, Davies Jet al., 2024,

  Levelling the playing field through the London Network of the UK clinical trials accelerator platform

  , Contemporary Clinical Trials Communications, Vol: 39, ISSN: 2451-8654

  Cystic fibrosis (CF) is a multisystem, genetic disease with a significantly reduced life expectancy. Despite substantial progress in therapies in the last 10–15 years, there is still no cure. There are dozens of drugs in the development pipeline and multiple clinical trials are being conducted across the globe. The UK Cystic Fibrosis Trust's (CFT) Clinical Trials Accelerator Platform (CTAP) is a national initiative bringing together 25 UK based CF centres to support the CF community in accessing and participating in CF clinical trials. CTAP enables more CF centres to run a broader portfolio of trials and increases the range of CF studies available for UK patients.There are four large specialist CF centres based in London, all within a small geographical region as well as two smaller centres which deliver CF care. At the launch of CTAP, these centres formed a sub-network in a consortium-style collaboration. The purpose of the network was to ensure equity of access to trials for patients across the UK's capital, and to share experience and knowledge. Four years into the programme we have reviewed our practices through working group meetings and an online survey. We sought to identify strengths and areas for improvement. We share our findings here, as we believe they are relevant to others delivering research in regions outside of London and in other chronic diseases.

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• Journal article
  Mainz JG, Lester K, Elnazir B, Williamson M, Mckone E, Cox D, Linnane B, Zagoya C, Duckstein F, Barucha A, Davies JC, Mcnally Pet al., 2024,

  Reduction in abdominal symptoms (CFAbd-Score), faecal M2-pyruvate-kinase and Calprotectin over one year of treatment with Elexacaftor-Tezacaftor-Ivacaftor in people with CF aged ≥12 years - The RECOVER study

  , JOURNAL OF CYSTIC FIBROSIS, Vol: 23, Pages: 474-480, ISSN: 1569-1993
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• Journal article
  Gramegna A, Addy C, Allen L, Bakkeheim E, Brown C, Daniels T, Davies G, Davies JC, De Marie K, Downey D, Felton I, Hafkemeyer S, Hamouda S, Kendall V, Lindberg U, Macek M, Mayell S, Pearlsman O, Schechter MS, Salvatori L, Sands D, Schwarz C, Shteinberg M, Taylor J, Taylor-Cousar JL, Taylor-Robinson D, Watkins B, Verkleij M, Bevan A, Castellani C, Drevinek P, Gartner S, Lammertyn E, Landau EEC, Middleton PG, Plant BJ, Smyth AR, van Koningsbruggen-Rietschel S, Burgel P-R, Southern KWet al., 2024,

  Standards for the care of people with cystic fibrosis (CF); Planning for a longer life

  , JOURNAL OF CYSTIC FIBROSIS, Vol: 23, Pages: 375-387, ISSN: 1569-1993
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