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  • Journal article
    Swieboda D, Guo Y, Sagawe S, Thwaites RS, Nadel S, Openshaw PJM, Culley FJet al., 2019,

    OMIP-062: A 14-Color, 16-antibody panel for immunophenotyping human innate yymphoid, myeloid and T cells in small volumes of whole blood and pediatric airway samples

    , Cytometry Part A, ISSN: 1552-4949

    This 14‐color, 16‐antibody OMIP was designed for enumeration of leukocyte responses in pediatric samples, where sample volumes and cell numbers can be very low. Leukocytes identified by this panel include all major members of the innate lymphoid cell (ILC) family (ILC1s, ILC2s, and ILC3s), natural killer cells (NK cells), granulocytes (neutrophils and eosinophils), T‐cells (CD4+ and CD8+), mucosal‐associated invariant T cells (MAIT cells) and NKT‐like cells. The protocol was optimized using small volumes of peripheral blood and validated in airway samples obtained from children (< 2 years of age) admitted to a pediatric intensive care unit (PICU). Given this backdrop, this OMIP is widely applicable to clinical research using low volume or paucicellular samples, such as studies of innate and adaptive immune responses in infants and children, with potential clinical application in diagnostics and monitoring of patients by pediatricians.

  • Conference paper
    Edmondson C, Westrupp N, Brownlee K, Wallenburg J, Alton E, Bush A, Davies JCet al., 2019,

    ENGAGEMENT (OR NOT) OF TEENAGERS WITH CF IN HEALTH MONITORING AT HOME: RESULTS FROM THE CLIMB-CF FEASABILITY STUDY

    , Publisher: WILEY, Pages: S430-S430, ISSN: 8755-6863
  • Conference paper
    Edmondson C, Westrupp N, Brownlee K, Wallenburg J, Alton E, Bush A, Davies JCet al., 2019,

    DOES HOME MONITORING OF CHILDREN WITH CF IMPACT DEPRESSION AND ANXIETY LEVELS IN THEIR PARENTS? RESULTS FROM THE CLIMB-CF FEASIBILITY STUDY

    , Publisher: WILEY, Pages: S405-S405, ISSN: 8755-6863
  • Conference paper
    Saleh A, Griesenbach U, Alton E, Sinadinos A, Meng Cet al., 2019,

    ASSAY DEVELOPMENT FOR A FIRST-IN-MAN LENTIVIRUS GENE THERAPY TRIAL FOR CYSTIC FIBROSIS

    , Publisher: WILEY, Pages: S358-S358, ISSN: 8755-6863
  • Conference paper
    Waller MD, Harman K, Bayfield KJ, Saunders C, Simmonds N, Davies JC, Alton Eet al., 2019,

    OPPORTUNISTIC ASSESSMENT OF UPPER AND LOWER AIRWAY ELECTROPHYSIOLOGY AND LUNG FUNCTION IN CYSTIC FIBROSIS

    , Publisher: WILEY, Pages: S163-S163, ISSN: 8755-6863
  • Journal article
    Jha A, Dunning J, Tunstall T, Thwaites R, Hoang L, The MOSAIC Investigators, Kon OM, Zambon MC, Hansel TT, Openshaw Pet al., 2019,

    Patterns of systemic and local inflammation in patients with asthma hospitalised with influenza

    , European Respiratory Journal, Vol: 54, ISSN: 0903-1936

    BackgroundPatients with asthma are at risk of hospitalisation with influenza, but the reasons for this predisposition are unknown.Study settingA prospective observational study of adults with PCR-confirmed influenza in 11 UK hospitals, measuring nasal, nasopharyngeal and systemic immune mediators and whole-blood gene expression.ResultsOf 133 admissions, 40 (30%) had previous asthma; these were more often female (70% vs 38.7%, OR 3.69, 95% CI 1.67 to 8.18, P = 0.0012), required less mechanical ventilation (15% vs 37.6%, χ2 6.78, P=0.0338) and had shorter hospital stays (mean 8.3 vs 15.3 d, P=0.0333) than those without. In patients without asthma, severe outcomes were more frequent in those given corticosteroids (OR=2.63, 95% CI=1.02-6.96, P=0.0466) or presenting >4 days after disease onset (OR 5.49, 95% CI 2.28–14.03, P=0.0002). Influenza vaccination in at-risk groups (including asthma) were lower than intended by national policy and the early use of antiviral medications were less than optimal. Mucosal immune responses were equivalent between groups. Those with asthma had higher serum IFN-α but lower serum TNF, IL-5, IL-6, CXCL8, CXCL9, IL-10, IL-17 and CCL2 levels (all P<0.05); both groups had similar serum IL-13, total IgE, periostin and blood eosinophil gene expression levels. Asthma diagnosis was unrelated to viral load, IFN-α, IFN-γ, IL-5 or IL-13 levels.ConclusionsAsthma is common in those hospitalised with influenza, but may not represent classical Type 2-driven disease. Those admitted with influenza tend to be female with mild serum inflammatory responses, increased serum IFN-α levels and good clinical outcomes.

  • Journal article
    Culley F, Swieboda D, Guo Y, Thwaites R, Nadel S, Openshaw Pet al.,

    A 14-color, 16-antibody panel for immunophenotyping human innate lymphoid, myeloid and T cells in small volumes of whole blood and pediatric airway samples

    , Cytometry Part A, ISSN: 1552-4949
  • Journal article
    Davies JC, Drevinek P, Elborn JS, Kerem E, Lee T, European CF Society ECFS Strategic Planning Task Force on Speeding up access to new 4 drugs for CF, Amaral MD, de Boeck K, Davies JC, Drevinek P, Elborn JS, Kerem E, Lee Tet al., 2019,

    Speeding up access to new drugs for CF: Considerations for clinical trial design and delivery

    , Journal of Cystic Fibrosis, Vol: 18, Pages: 677-684, ISSN: 1569-1993

    The last decade has witnessed developments in the CF drug pipeline which are both exciting and unprecedented, bringing with them previously unconsidered challenges. The Task Force group was brought together to consider these challenges and possible strategies to address them. Over the last 18 months, we have discussed internally and gathered views from a broad range of individuals representing patient organisations, clinical and research teams, the pharmaceutical industry and regulatory agencies. In this and the accompanying article, we discuss two main areas of focus: i) optimising trial design and delivery for speed and efficiency; ii) drug development for patients with rare CFTR mutations. We propose some strategies to tackle the challenges ahead and highlight areas where further thought is needed. We see this as the start of a process rather than the end and hope herewith to engage the wider community in seeking solutions to improved treatments for all patients with CF.

  • Journal article
    Kirsebom FCM, Kausar F, Nuriev R, Makris S, Johansson Cet al., 2019,

    Neutrophil recruitment and activation are differentially dependent on MyD88/TRIF and MAVS signaling during RSV infection

    , Mucosal Immunology, Vol: 12, Pages: 1244-1255, ISSN: 1933-0219

    Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infections, especially in infants. Lung neutrophilia is a hallmark of RSV disease but the mechanism by which neutrophils are recruited and activated is unclear. Here, we investigate the innate immune signaling pathways underlying neutrophil recruitment and activation in RSV-infected mice. We show that MyD88/TRIF signaling is essential for lung neutrophil recruitment while MAVS signaling, leading to type I IFN production, is necessary for neutrophil activation. Consistent with that notion, administration of type I IFNs to the lungs of RSV-infected Mavs-/- mice partially activates lung neutrophils recruited via the MyD88/TRIF pathway. Conversely, lack of neutrophil recruitment to the lungs of RSV-infected Myd88/Trif-/- mice can be reversed by administration of chemoattractants and those neutrophils become fully activated. Interestingly, Myd88/Trif-/- mice did not have increased lung RSV loads during infection, suggesting that neutrophils are dispensable for control of the virus. Thus, two distinct pathogen sensing pathways collaborate for neutrophil recruitment and full activation during RSV infection.

  • Journal article
    Davies JC, Scott S, Dobra R, Brendell R, Brownlee K, Carr SB, Cosgriff R, Simmonds NJ, London Network of Clinical Trials Accelerator Platform sites, Jahan R, Jones A, Matthews J, Brown S, Galono K, Miles K, Pao C, Shafi N, Watson D, Orchard C, Davies G, Pike K, Shah S, Bossley CJ, Fong T, Macedo P, Ruiz G, Waller M, Baker Let al., 2019,

    Fair selection of participants in clinical trials: The challenge to push the envelope further.

    , J Cyst Fibros, Vol: 18, Pages: e48-e50

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

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