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  • Journal article
    Philip K, Lewis A, Hopkinson NS, 2019,

    Music and dance in chronic lung disease

    , Breathe, Vol: 15, Pages: 116-120, ISSN: 1810-6838

    Arts in Health interventions show potential to improve the quality of life of people with chronic lung disease. Listening to music, making music, and dance have accepted and established roles in the lives of people without chronic disease. However, their potential utility in chronic disease management is infrequently considered by medical professionals. The aim of this review is to examine the use of music and dance in the treatment and self-management of chronic lung disease. Although the evidence base is currently limited, existing research suggests a range of biopsychosocial benefits. As personalised medicine and social prescribing become more prominent, further research is required to establish the role of arts interventions in chronic lung disease.

  • Journal article
    Laverty AA, Filippidis FT, Taylor-Robinson D, Millett C, Bush A, Hopkinson NSet al., 2019,

    Smoking uptake in UK children: Analysis of the UK Millennium Cohort Study.

    , Thorax, Vol: 74, Pages: 607-610, ISSN: 0040-6376

    We used data from 11 577 children in the UK Millennium Cohort Study, collected at approximately 14 years of age (early teens), to assess characteristics associated with smoking, and generated regional estimates of numbers of smokers. 13.8% of UK early teens studied had ever smoked; 1.9% were current smokers. This corresponds to 2 28 136 and 39 653 (13-14 year olds) in the UK, respectively. Ever smoking risk increased if caregivers (26.0% vs 10.9%) or friends smoked (35.1% vs 4.0%), with a dose-response effect for friends' smoking. Caregiver and peer-group smoking remain important drivers of child smoking uptake and thus important targets for intervention.

  • Journal article
    Benedikz EK, Bailey D, Cook CNL, Goncalves-Carneiro D, Buckner MMC, Blair JMA, Wells TJ, Fletcher NF, Goodall M, Flores-Langarica A, Kingsley RA, Madsen J, Teeling J, Johnston SL, MacLennan CA, Balfe P, Henderson IR, Piddock LJV, Cunningham AF, McKeating JAet al., 2019,

    Bacterial flagellin promotes viral entry via an NF-kB and Toll Like Receptor 5 dependent pathway

    , SCIENTIFIC REPORTS, Vol: 9, ISSN: 2045-2322
  • Journal article
    Sharanya A, Ciano M, Withana S, Polkey M, Kemp P, Natanek Set al., 2019,

    Sex differences in COPD-related quadriceps muscle dysfunction and fibre abnormalities

    , Chronic Respiratory Disease, Vol: 16, Pages: 1-13, ISSN: 1479-9723

    Background: In COPD, lower limb dysfunction is associated with reduced exercise capacity, increased hospitalisations and mortality. We investigated sex differences in the prevalence of quadriceps dysfunction and fibre abnormalities in a large COPD cohort, controlling for the normal sex differences in health. Methods: We compared existing data from 76 male and 38 female COPD patients where each variable was expressed as a function of gender-specific normal values (obtained from 16 male and 14 female controls). Results: Female COPD patients had lower quadriceps muscle strength and peak workload on a maximal incremental cycle ergometry protocol compared to male patients. Female patients had a smaller type II fibre cross-sectional area (CSA) compared to male patients, suggesting a greater female preponderance to fibre atrophy, although this result was largely driven by a few male patients with increased type II fibre CSA. Female patients had significantly higher concentrations of a number of plasma pro-inflammatory cytokines including tumor necrosis factor alpha (TNFα) and interleukin 8 (IL8), but not lower levels of physical activity or arterial oxygenation, compared to males. Conclusions: Our data confirms results from a previous small study and suggests that female COPD patients have a greater prevalence of muscle wasting and weakness. Larger studies investigating sex differences in COPD-related muscle atrophy and weakness are needed, as the results will have implications for monitoring in clinical practice and for design of clinical trials evaluating novel muscle anabolic agents.

  • Journal article
    Singh D, Agusti A, Anzueto A, Barnes PJ, Bourbeau J, Celli BR, Criner GJ, Frith P, Halpin DMG, Han M, López Varela MV, Martinez F, Montes de Oca M, Papi A, Pavord ID, Roche N, Sin DD, Stockley R, Vestbo J, Wedzicha JA, Vogelmeier Cet al., 2019,

    Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease: The GOLD Science Committee Report 2019

    , European Respiratory Journal, Vol: 53, ISSN: 0903-1936

    Precision medicine is a patient specific approach that integrates all relevant clinical, genetic and biological information in order to optimise the therapeutic benefit relative to the possibility of side effects for each individual. Recent clinical trials have shown that higher blood eosinophil counts are associated with a greater efficacy of inhaled corticosteroids (ICS) in COPD patients. Blood eosinophil counts are a biomarker with potential to be used in clinical practice, to help target ICS treatment with more precision in COPD patients with a history of exacerbations despite appropriate bronchodilator treatment.The Global initiative for the management of chronic Obstructive Lung Disease (GOLD) 2017 pharmacological treatment algorithms, based on the ABCD assessment, can be applied relatively easily to treatment naïve individuals at initial presentation. However, their use is more problematic during follow up in patients who are already on maintenance treatment. There is a need for a different system to guide COPD pharmacological management during follow up.Recent large randomised controlled trials have provided important new information concerning the therapeutic effects of ICS and long-acting bronchodilators on exacerbations. The new evidence regarding blood eosinophils and inhaled treatments, and the need to distinguish between initial and follow up pharmacological management, led to changes in the GOLD pharmacological treatment recommendations. This paper explains the evidence and rationale for the GOLD 2019 pharmacological treatment recommendations.

  • Journal article
    Postma DS, Brightling C, Baldi S, Van den Berge M, Fabbri LM, Gagnatelli A, Papi A, Van der Molen T, Rabe KF, Siddiqui S, Singh D, Nicolini G, Kraft M, ATLANTIS study groupet al., 2019,

    Exploring the relevance and extent of small airways dysfunction in asthma (ATLANTIS): baseline data from a prospective cohort study.

    , Lancet Respir Med, Vol: 7, Pages: 402-416

    BACKGROUND: Small airways dysfunction (SAD) is well recognised in asthma, yet its role in the severity and control of asthma is unclear. This study aimed to assess which combination of biomarkers, physiological tests, and imaging markers best measure the presence and extent of SAD in patients with asthma. METHODS: In this baseline assessment of a multinational prospective cohort study (the Assessment of Small Airways Involvement in Asthma [ATLANTIS] study), we recruited participants with and without asthma (defined as Global Initiative for Asthma severity stages 1-5) from general practices, the databases of chest physicians, and advertisements at 29 centres across nine countries (Brazil, China, Germany, Italy, Spain, the Netherlands, the UK, the USA, and Canada). All participants were aged 18-65 years, and participants with asthma had received a clinical diagnosis of asthma more than 6 months ago that had been confirmed by a chest physician. This diagnosis required support by objective evidence at baseline or during the past 5 years, which could be: positive airway hyperresponsiveness to methacholine, positive reversibility (a change in FEV1 ≥12% and ≥200 mL within 30 min) after treatment with 400 μg of salbutamol in a metered-dose inhaler with or without a spacer, variability in peak expiratory flow of more than 20% (measured over 7 days), or documented reversibility after a cycle (eg, 4 weeks) of maintenance anti-asthma treatment. The inclusion criteria also required that patients had stable asthma on any previous regular asthma treatment (including so-called rescue β2-agonists alone) at a stable dose for more than 8 weeks before baseline and had smoked for a maximum of 10 pack-years in their lifetime. Control group participants were recruited by advertisements; these participants were aged 18-65 years, had no respiratory symptoms compatible with asthma or chronic obstructive pulmonary disease, normal spirometry, and normal airways responsiveness, an

  • Journal article
    Cryer AM, Chan C, Eftychidou A, Maksoudian C, Mahesh M, Tetley TD, Spivey AC, Thorley AJet al., 2019,

    Tyrosine kinase inhibitor gold nanoconjugates for the treatment of non-small cell lung cancer

    , ACS Applied Materials and Interfaces, Vol: 11, Pages: 16336-16346, ISSN: 1944-8244

    Gold nanoparticles (AuNPs) have emerged as promising drug delivery candidates that can be leveraged for cancer therapy. Lung cancer (LC) is a heterogeneous disease that imposes a significant burden on society, with an unmet need for new therapies. Chemotherapeutic drugs such as afatinib (Afb), which is clinically approved for the treatment of epidermal growth factor receptor positive LC, is hydrophobic and has low bioavailability leading to spread around the body, causing severe side effects. Herein, we present a novel afatinib-AuNP formulation termed Afb-AuNPs, with the aim of improving drug efficacy and biocompatibility. This was achieved by synthesis of an alkyne-bearing Afb derivative and reaction with azide functionalized lipoic acid using copper catalyzed click chemistry, then conjugation to AuNPs via alkylthiol-gold bond formation. The Afb-AuNPs were found to possess up to 3.7-fold increased potency when administered to LC cells in vitro and were capable of significantly inhibiting cancer cell proliferation, as assessed by MTT assay and electric cell-substrate impedance sensing respectively. Furthermore, when exposed to Afb-AuNPs, human alveolar epithelial type I-like cells, a model of the healthy lung epithelium, maintained viability and were found to release less pro-inflammatory cytokines when compared to free drug, demonstrating the biocompatibility of our formulation. This study provides a new platform for the development of non-traditional AuNP conjugates which can be applied to other molecules of therapeutic or diagnostic utility, with potential to be combined with photothermal therapy in other cancers.

  • Journal article
    Calderazzo MA, Trujillo-Torralbo M-B, Finney LJ, Singanayagam A, Bakhsoliani E, Padmanaban V, Kebadze T, Aniscenko J, Elkin SL, Johnston SL, Mallia Pet al., 2019,

    Inflammation and infections in unreported chronic obstructive pulmonary disease exacerbations

    , International Journal of Chronic Obstructive Pulmonary Disease, Vol: 2019, Pages: 823-832, ISSN: 1176-9106

    Purpose: COPD patients often do not report acute exacerbations to healthcare providers – unreported exacerbations. It is not known whether variances in symptoms, airway obstruction, aetiology and inflammatory responses account for differences in reporting of COPD exacerbations. The aims of the study were to compare symptoms, lung function changes, aetiology and inflammatory markers between exacerbations that were reported to healthcare providers or treated, with those that were unreported and untreated.Patients and methods: We recruited a cohort of COPD patients and collected clinical data and blood and airway samples when stable and during acute exacerbations. Virological and bacterial analyses were carried out and inflammatory markers measured.Results: We found no differences in symptoms, lung function, incidence of infection and inflammatory markers between reported and unreported exacerbations. Subjects who reported all exacerbations had higher BODE scores, lower FEV1 and more exacerbations compared with those who did not.Conclusion: The failure to report exacerbations is not related to the severity, aetiology or inflammatory profile of the exacerbation. Patients with less severe COPD and less frequent exacerbations are less likely to report exacerbations. The decision to report an exacerbation is not an objective marker of exacerbation severity and therefore studies that do not count unreported exacerbations will underestimate the frequency of clinically significant exacerbations. A better understanding of the factors that determine non-reporting of exacerbations is required to improve exacerbation reporting.

  • Journal article
    Smitten KL, Southam HM, de la Serna JB, Gill MR, Jarman PJ, Smythe CGW, Poole RK, Thomas JAet al., 2019,

    Using Nanoscopy To Probe the Biological Activity of Antimicrobial Leads That Display Potent Activity against Pathogenic, Multidrug Resistant, Gram-Negative Bacteria.

    , ACS Nano

    Medicinal leads that are also compatible with imaging technologies are attractive, as they facilitate the development of therapeutics through direct mechanistic observations at the molecular level. In this context, the uptake and antimicrobial activities of several luminescent dinuclear RuII complexes against E. coli were assessed and compared to results obtained for another ESKAPE pathogen, the Gram-positive major opportunistic pathogen Enterococcus faecalis, V583. The most promising lead displays potent activity, particularly against the Gram-negative bacteria, and potency is retained in the uropathogenic multidrug resistant EC958 ST131 strain. Exploiting the inherent luminescent properties of this complex, super-resolution STED nanoscopy was used to image its initial localization at/in cellular membranes and its subsequent transfer to the cell poles. Membrane damage assays confirm that the complex disrupts the bacterial membrane structure before internalization. Mammalian cell culture and animal model studies indicate that the complex is not toxic to eukaryotes, even at concentrations that are several orders of magnitude higher than its minimum inhibitory concentration (MIC). Taken together, these results have identified a lead molecular architecture for hard-to-treat, multiresistant, Gram-negative bacteria, which displays activities that are already comparable to optimized natural product-based leads.

  • Journal article
    Smith JA, McGarvey L, Morice AH, Birring SS, Wedzicha JA, Notari M, Zapata A, Segarra R, Seoane B, Jarreta Det al., 2019,

    The Effect of Aclidinium on Symptoms Including Cough in COPD: A Phase IV, DoubleBlind, Placebo-Controlled, Parallel-Group Study.

    , Am J Respir Crit Care Med
  • Journal article
    Dunne A, Kawamatawong T, Fenwick P, Davies C, Tullett H, Barnes P, Donnelly Let al., 2019,

    Direct inhibitory rffect of the phosphodiesterase-4 inhibitor, roflumilast, on neutrophil migration in COPD

    , American Journal of Respiratory Cell and Molecular Biology, Vol: 60, Pages: 445-453, ISSN: 1044-1549

    Neutrophilic inflammation is characteristic of COPD, yet there are no effective anti-inflammatory therapies. The phosphodiesterase (PDE)4 inhibitor, roflumilast is approved for use in COPD and suppresses sputum neutrophilia. The mechanism underlying this observation is unclear and therefore this study addressed whether roflumilast directly affected neutrophil migration. Blood-derived neutrophils were isolated from non-smokers, smokers and COPD patients and chemotaxis measured using Boyden chambers. Intracellular calcium ion concentration ([Ca2+]i) was measured by fluorimetry and shape change and CD11b expression by flow cytometry. Neutrophils from COPD patients showed enhanced chemotactic responses towards both CXCL1 and LTB4 compared with control cells. Chemotaxis was inhibited by both the active metabolite, roflumilast-N-oxide, and rolipram in a concentration-dependent manner with no difference in responsiveness between subjects. Roflumilast-N-oxide and rolipram were less efficacious against CXCL1 and LTB4-mediated [Ca2+]i suggesting that inhibition was not via this pathway. Both PDE4 inhibitors attenuated chemoattractant-mediated shape change and CD11b up-regulation suggesting common mechanisms. The stable cAMP analogue, 8-Br-cAMP, inhibited chemotaxis, as did the direct Epac1 activator 8-pCPT-2’-O-Me-cAMP but not the direct PKA activator, 6-Bnz-cAMP. These data suggest that roflumilast inhibits neutrophil chemotaxis directly via a cAMP-mediated mechanism requiring activation of Epac1, and that Epac1 activators could reduce COPD neutrophilic inflammation.

  • Journal article
    Donaldson GC, Witt C, Näyhä S, 2019,

    Changes in cold-related mortalities between 1995 and 2016 in South East England

    , Public Health, Vol: 169, Pages: 36-40, ISSN: 0033-3506

    OBJECTIVE: The aim of the study was to examine trends in cold-related mortalities between 1995 and 2016. STUDY DESIGN: This is a longitudinal mortality study. METHODS: For men and women aged 65-74 years or those older than 85 years in South East England, the relationship between daily mortality (deaths per million population) and outdoor temperatures below 18 °C, with allowance for influenza epidemics, was assessed by linear regression on an annual basis. The regression coefficients were expressed as a percentage of the mortality at 18 °C to adjust for changes in mortality through health care. Trends in 'specific' cold-related mortalities were then examined over two periods, 1977-1994 and 1995-2016. RESULTS: In contrast to the early period, annual trends in cold-related specific mortalities showed no decline between 1995 and 2016. 'Specific' cold-related mortality of women, but not men, in the age group older than 85 years showed a significant increase over the 1995-2016 period, which was different from the trend over the earlier period (P < 0.01). CONCLUSION: Despite state-funded benefits to help alleviate fuel poverty and public health advice, very elderly women appear to be at increasing risk of cold-related mortality-greater help may be necessary.

  • Journal article
    Potaczek DP, Unger SD, Zhang N, Taka S, Michel S, Akdag N, Lan F, Helfer M, Hudemann C, Eickmann M, Skevaki C, Megremis S, Sadewasser A, Alhamwe BA, Alhamdan F, Akdis M, Edwards MR, Johnston SL, Akdis CA, Becker S, Bachert C, Papadopoulos NG, Garn H, Renz Het al., 2019,

    Development and characterization of DNAzyme candidates demonstrating significant efficiency against human rhinoviruses

    , JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 143, Pages: 1403-1415, ISSN: 0091-6749
  • Journal article
    Wang M, Zhang Y, Xu M, Zhang H, Chen Y, Chung KF, Adcock IM, Li Fet al., 2019,

    Roles of TRPA1 and TRPV1 in cigarette smoke -induced airway epithelial cell injury model

    , Free Radical Biology and Medicine, Vol: 134, Pages: 229-238, ISSN: 0891-5849

    Transient receptor potential protein (TRP) ion channels TRPA1 and TRPV1 may be important in mediating airway tissue injury and inflammation. This study was designed to clarify the role of TRPA1 and TRPV1 channels in cigarette smoke extract (CSE)-induced damage to bronchial and alveolar epithelial cells. Alveolar epithelial (A549) cells and bronchial epithelial (Beas-2B) cells were treated with CSE in the presence and absence of a TRPA1 inhibitor (100 μM, A967079), a TRPV1 inhibitor (100 μM, AMG9810) or both. DCFH-DA and MitoSOX Red probes were used to assay intracellular and mitochondrial oxidative stress, respectively. The mRNA levels of inflammatory mediators (IL-1β, IL-8, IL-18, IL-33) and antioxidants (HO-1, NQO1, MnSOD, catalase) and the protein expression levels of mitochondrial and inflammasome factors (MFN2, OPA1, DRP1, MFF, NLRP3,caspase-1) were respectively detected by RT-PCR and Western Blot. The results were validated in TRPA1 shRNA and TRPV1 shRNA cells. In both cell types, 10% CSE increased intracellular and mitochondrial oxidative stress, induced Ca2+ influx, increased inflammatory gene expression, reduced antioxidant gene expression and inhibited the activities of mitochondrial respiratory chain (MRC) complexes. 10% CSE increased the expression of mitochondrial fission proteins (MFF and DRP1), Caspase-1 and NLRP3 protein expression and decreased that of mitochondrial fusion proteins (MFN2 and OPA1). Both inhibitors and gene-knockout of TRPA1 and TRPV1 reduced oxidative stress, blocked Ca2+ influx, and inhibited inflammatory and increased antioxidant gene expression. They also prevented the changes in mitochondrial fission and fusion proteins and in MRC complexes activities induced by CSE. Both TRPA1 and TRPV1 mediate CSE-induced damage of bronchial and alveolar epithelial cells via modulation of oxidative stress, inflammation and mitochondrial damage and their inhibition should be considered as potential therapy for COPD.

  • Journal article
    Ravanetti L, Dijkhuis A, Dekker T, Sabogal Pineros YS, Ravi A, Dierdorp BS, Erjefält JS, Mori M, Pavlidis S, Adcock IM, Rao NL, Lutter Ret al., 2019,

    IL-33 drives influenza-induced asthma exacerbations by halting innate and adaptive anti-viral immunity

    , Journal of Allergy and Clinical Immunology, Vol: 143, Pages: 1355-1370, ISSN: 0091-6749

    BACKGROUND: Influenza virus triggers severe exacerbations of asthma for which no adequate treatment is available. It is known that IL-33 levels correlate with exacerbation severity, but its role in the immune-pathogenesis of exacerbations has remained elusive. OBJECTIVE: We hypothesized that IL-33 is necessary to drive asthma exacerbations. We intervened with the IL-33 cascade and sought to dissect its role, also in synergy with TSLP, in airway inflammation, anti-viral activity and lung function. We aimed to unveil the major source of IL-33 in the airways and IL-33-dependent mechanisms that underlie severe asthma exacerbation. METHODS: Mild asthmatic patients were experimentally infected with rhinovirus. Mice were chronically exposed to house dust mite (HDM) extract and then infected with influenza to resemble key features of exacerbations in humans. Interventions included anti-IL-33-receptor ST2 and/or anti-TSLP. RESULTS: We identified bronchial ciliated cells and Type-II alveolar cells as a major local source of IL-33 during virus-driven exacerbation in humans and mice, respectively. By blocking ST2 we demonstrated that IL-33 and not TSLP was necessary to drive exacerbations. IL-33 enhanced AHR and airway inflammation by suppressing innate and adaptive anti-viral responses and by instructing epithelial cells and dendritic cells (DCs) of HDM-sensitized mice to dampen IFN-β expression and prevent the Th1-promoting DCs phenotype. IL-33 also boosted luminal NETosis and halted cytolytic anti-viral activities, but did not affect the Th2-response. CONCLUSION: Interventions targeting the IL-33/ST2 axis could prove an effective acute, short-term therapy for virus-induced asthma exacerbation.

  • Journal article
    Bousquet J, Bedbrook A, Czarlewski W, Onorato GL, Arnavielhe S, Laune D, Mathieu-Dupas E, Fonseca J, Costa E, Lourenco O, Morais-Almeida M, Todo-Bom A, Illario M, Menditto E, Canonica GW, Cecchi L, Monti R, Napoli L, Ventura MT, De Feo G, Fokkens WJ, Chavannes NH, Reitsma S, Cruz AA, da Silva J, Serpa FS, Larenas-Linnemann D, Perez JMF, Huerta-Villalobos YR, Rivero-Yeverino D, Rodriguez-Zagal E, Valiulis A, Dubakiene R, Emuzyte R, Kvedariene V, Annesi-Maesano I, Blain H, Bonniaud P, Bosse I, Dauvilliers Y, Devillier P, Fontaine JF, Pepin JL, Pham-Thi N, Portejoie F, Picard R, Roche N, Rolland C, Schmidt-Grendelmeier P, Kuna P, Samolinski B, Anto JM, Cardona V, Mullol J, Pinnock H, Ryan D, Sheikh A, Walker S, Williams S, Becker S, Klimek L, Pfaar O, Bergmann KC, Mosges R, Zuberbier T, Roller-Wirnsberger RE, Tomazic PV, Haahtela T, Salimaki J, Toppila-Salmi S, Valovirta E, Vasankari T, Gemicioglu B, Yorgancioglu A, Papadopoulos NG, Prokopakis EP, Tsiligianni IG, Bosnic-Anticevich S, O'Hehir R, Ivancevich JC, Neffen H, Zernotti ME, Kull I, Melen E, Wickman M, Bachert C, Hellings PW, Brusselle G, Palkonen S, Bindslev-Jensen C, Eller E, Waserman S, Boulet LP, Bouchard J, Chu DK, Schunemann HJ, Sova M, De Vries G, van Eerd M, Agache I, Ansotegui IJ, Bewick M, Casale T, Dykewick M, Ebisawa M, Murray R, Naclerio R, Okamoto Y, Wallace DV, Bousquet J, Hellings PW, Aberer W, Agache I, Akdis CA, Akdis M, Aliberti MR, Almeida R, Amat F, Angles R, Annesi-Maesano I, Ansotegui IJ, Anto JM, Arnavielle S, Asayag E, Asarnoj A, Arshad H, Avolio F, Bacci E, Bachert C, Baiardini I, Barbara C, Barbagallo M, Baroni I, Barreto BA, Basagana X, Bateman ED, Bedolla-Barajas M, Bedbrook A, Bewick M, Beghe B, Bel EH, Bergmann KC, Bennoor KS, Benson M, Bertorello L, Bialoszewski AZ, Bieber T, Bialek S, Bindslev-Jensen C, Bjermer L, Blain H, Blasi F, Blua A, Marciniak MB, Bogus-Buczynska I, Boner AL, Bonini M, Bonini S, Bosnic-Anticevich CS, Bosse I, Bouchard J, Boulet LP, Bourret R, Bousquet PJ Bet al., 2019,

    Guidance to 2018 good practice: ARIA digitally-enabled, integrated, person-centred care for rhinitis and asthma


    AimsMobile Airways Sentinel NetworK (MASK) belongs to the Fondation Partenariale MACVIA-LR of Montpellier, France and aims to provide an active and healthy life to rhinitis sufferers and to those with asthma multimorbidity across the life cycle, whatever their gender or socio-economic status, in order to reduce health and social inequities incurred by the disease and to improve the digital transformation of health and care. The ultimate goal is to change the management strategy in chronic diseases.MethodsMASK implements ICT technologies for individualized and predictive medicine to develop novel care pathways by a multi-disciplinary group centred around the patients.StakeholdersInclude patients, health care professionals (pharmacists and physicians), authorities, patient’s associations, private and public sectors.ResultsMASK is deployed in 23 countries and 17 languages. 26,000 users have registered.

  • Journal article
    Agusti A, Faner R, Donaldson G, Heuvelin E, Breyer-Kohansal R, Melén E, Maitland-van der Zee AH, Vestbo J, Allinson JP, Vanfleteren LEGW, van den Berge M, Adcock IM, Lahousse L, Brusselle G, Wedzicha JA, onbehalf of the CADSET Clinical Research Collaboration, Current members of the CADSET Clinical Research Collaborationet al., 2019,

    Chronic Airway Diseases Early Stratification (CADSET): a new ERS Clinical Research Collaboration

    , European Respiratory Journal, Vol: 53, ISSN: 0903-1936

    A recent editorial in the European Respiratory Journal highlighted the strategic importance of the Clinical Research Collaborations (CRCs) launched in 2013 by the European Respiratory Society (ERS) [1]. These have the aim of 1) promoting the exchange of research ideas among clinicians and affiliated scientists in Europe and/or globally; 2) building an infrastructure for prospective clinical research; 3) securing additional funding through national and European Union funding streams; and 4) facilitating the planning, implementation, evaluation and publication of clinical and translational studies at pan-European level and beyond. So far, there are currently 17 ongoing CRCs that cover eight major respiratory disease domains (airway diseases, interstitial lung diseases, pulmonary vascular diseases, sleep and breathing disorders, respiratory critical care, paediatric respiratory diseases, respiratory infections and thoracic oncology), all of them linked to one or more ERS assemblies [2–12]. CADSET, an acronym that stands for “Chronic Airway Diseases Early Stratification”, is the latest addition to the list of ongoing CRCs ( This editorial presents the rationale, goals and research strategy for CADSET.

  • Journal article
    Bousquet J, Hellings PW, Agache I, Amat F, Annesi-Maesano I, Ansotegui IJ, Anto JM, Bachert C, Bateman ED, Bedbrook A, Bennoor K, Bewick M, Bindslev-Jensen C, Bosnic-Anticevich S, Bosse I, Brozek J, Brussino L, Canonica GW, Cardona V, Casale T, Sarabia AMC, Chavannes NH, Cecchi L, de Sousa JC, Costa E, Cruz AA, Czarlewski W, De Carlo G, De Feo G, Demoly P, Devillier P, Dykewicz MS, El-Gamal Y, Eller EE, Fonseca JA, Fontaine J-F, Fokkens WJ, Guzman M-A, Haahtela T, Illario M, Ivancevich J-C, Just J, Kaidashev I, Khaitov M, Kalayci O, Keil T, Klimek L, Kowalski ML, Kuna P, Kvedariene V, Larenas-Linnemann D, Laune D, Le LTT, Carlsen KL, Lourenco O, Mahboub B, Mair A, Menditto E, Milenkovic B, Morais-Almeida M, Mosges R, Mullol J, Murray R, Naclerio R, Namazova-Baranova L, Novellino E, O'Hehir RE, Ohta K, Okamoto Y, Okubo K, Onorato GL, Palkonen S, Panzner P, Papadopoulos NG, Park H-S, Paulino E, Pawankar R, Pfaar O, Plavec D, Popov TA, Potter P, Prokopakis EP, Rottem M, Ryan D, Salimaki J, Samolinski B, Sanchez-Borges M, Schunemann HJ, Sheikh A, Sisul J-C, Rajabian-Soderlund R, Sooronbaev T, Stellato C, To T, Todo-Bom A-M, Tomazic P-V, Toppila-Salmi S, Valero A, Valiulis A, Valovirta E, Ventura M-T, Wagenmann M, Wang DY, Wallace D, Waserman S, Wickman M, Yorgancioglu A, Zhang L, Zhong N, Zidarn M, Zuberbier T, Bousquet J, Hellings PW, Aberer W, Agache I, Akdis CA, Akdis M, Alberti MR, Almeida R, Amat F, Angles R, Annesi-Maesano I, Ansotegui IJ, Anto JM, Arnavielle S, Asayag E, Asarnoj A, Arshad H, Avolio F, Bacci E, Bachert C, Baiardini I, Barbara C, Barbagallo M, Baroni I, Barreto BA, Basagana X, Bateman ED, Bedolla-Barajas M, Bedbrook A, Bewick M, Beghe B, Bel EH, Bergmann KC, Bennoor KS, Benson M, Bertorello L, Biaoszewski AZ, Bieber T, Bialek S, Bindslev-Jensen C, Bjermer L, Blain H, Blasi F, Blua A, Marciniak MB, Bogus-Buczynska I, Boner AL, Bonini M, Bonini S, Bosnic-Anticevich CS, Bosse I, Bouchard J, Boulet LP, Bourret R, Bousquet PJ, Braido F, Briedis V, Brighet al., 2019,

    Allergic Rhinitis and its Impact on Asthma (ARIA) Phase 4 (2018): Change management in allergic rhinitis and asthma multimorbidity using mobile technology

    , Journal of Allergy and Clinical Immunology, Vol: 143, Pages: 864-879, ISSN: 0091-6749

    Allergic Rhinitis and its Impact on Asthma (ARIA) has evolved from a guideline by using the best approach to integrated care pathways using mobile technology in patients with allergic rhinitis (AR) and asthma multimorbidity. The proposed next phase of ARIA is change management, with the aim of providing an active and healthy life to patients with rhinitis and to those with asthma multimorbidity across the lifecycle irrespective of their sex or socioeconomic status to reduce health and social inequities incurred by the disease. ARIA has followed the 8-step model of Kotter to assess and implement the effect of rhinitis on asthma multimorbidity and to propose multimorbid guidelines. A second change management strategy is proposed by ARIA Phase 4 to increase self-medication and shared decision making in rhinitis and asthma multimorbidity. An innovation of ARIA has been the development and validation of information technology evidence-based tools (Mobile Airways Sentinel Network [MASK]) that can inform patient decisions on the basis of a self-care plan proposed by the health care professional.

  • Journal article
    Wilkinson A, Hillman T, Hopkinson NS, Janson C, Smith J, Woodcock AAet al., 2019,

    Our patients and our planet-holistic considerations for inhaler choice

    , Lancet Respiratory Medicine, Vol: 7, Pages: e11-e11, ISSN: 2213-2600
  • Journal article
    Pfeffer PE, Donaldson GC, Mackay AJ, Wedzicha JAet al., 2019,

    Increased COPD exacerbations of likely viral etiology follow elevated ambient nitrogen oxides

    , American Journal of Respiratory and Critical Care Medicine, Vol: 199, ISSN: 1073-449X

    RATIONALE: Epidemiological research strongly supports an association between air pollution and COPD exacerbations. Numerous mechanisms may underlie any association as pollutants are toxic to pulmonary cells and may increase susceptibility to respiratory infections. The relationship between ambient pollution and exacerbation etiology has not been studied. OBJECTIVES: To evaluate the characteristics of pollution-associated exacerbations and whether the association is specific to exacerbations of infective or non-infective etiology. METHODS: We analyzed the effect of preceding ambient PM10, NOx and O3 on characterized COPD exacerbations in a regression model adjusted for temperature, seasonality and long-term trend. We specifically examined associations with exacerbations of suspected viral and/or bacterial, or non-infective etiology. For the associations identified we further examined the characteristics of pollution-associated exacerbations. MEASUREMENTS AND MAIN RESULTS: 4173 exacerbations occurred over the 20 year study period. Higher ambient NOx was consistently associated with increased viral-type exacerbations at 2-4 days lag (p=0.010). Recovery for viral-type exacerbations following higher ambient NOx was significantly prolonged. These findings were consistent in the subset of 2841 exacerbations treated with oral corticosteroids or antibiotics, with recovery 1.29 (95% CI 1-17-1.42; P<0.001) times longer with 'viral-type' exacerbations of onset 3 days after above versus below median ambient NOx. A likely bimodal association of PM10 with infective exacerbations was also evident, and supported by a daily time-series analysis. CONCLUSIONS: Higher levels of ambient NOx are associated with prolonged exacerbations of likely viral etiology, supporting toxicological effects of air pollution that increase susceptibility to, and severity of, infection.

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