Publications
2409 results found
Ombredane HCJ, Fenwick PS, Barnes PJ, et al., 2023, Temporal Release of IL-1 Family Members from Virally Infected Airway Epithelial Cells Suggests IL-36γ Is the Early Responder., Am J Respir Cell Mol Biol, Vol: 68, Pages: 339-341
Ahmad S, Mohd Noor N, Engku Nur Syafirah EAR, et al., 2023, Anti-Tumor Necrosis Factor for Supplementary Management in Severe Asthma: A Systematic Review and Meta-analysis., J Interferon Cytokine Res, Vol: 43, Pages: 77-85
Tumor-necrosis factor (TNF) is recognized as a therapeutic target in inflammatory diseases, including asthma. In severe forms of asthma, biologics such as anti-TNF are rendered to be investigated as therapeutic options in severe asthma. Hence, this work is done to assess the efficacy and safety of anti-TNF as a supplementary therapy for patients with severe asthma. A systematic search of 3 databases (Cochrane Central Register of Controlled Trials, MEDLINE, ClinicalTrials.gov) was performed to identify for published and unpublished randomized controlled trials comparing anti-TNF (etanercept, adalimumab, infliximab, certolizumab pegol, golimumab) with placebo in patients diagnosed with persistent or severe asthma. Random-effects model was used to estimate risk ratios and mean differences (MDs) with confidence intervals (95% CIs). PROSPERO registration number is CRD42020172006. Four trials with 489 randomized patients were included. Comparison between etanercept and placebo involved 3 trials while comparison between golimumab and placebo involved 1 trial. Etanercept produced a small but significant impairment in forced expiratory flow in 1 second (MD 0.33, 95% CI 0.09-0.57, I2 statistic = 0%, P = 0.008) and a modest improvement of asthma control using the Asthma Control Questionnaire. However, using the Asthma Quality of Life Questionnaire, the patients exhibit an impaired quality of life with etanercept. Treatment with etanercept showed a reduced injection site reaction and gastroenteritis compared with placebo. Although treatment with anti-TNF is shown to improve asthma control, severe asthma patients did not benefit from this therapy as there is limited evidence for improvement in lung function and reduction of asthma exacerbation. Hence, it is unlikely to prescribe anti-TNF in adults with severe asthma.
Pavord ID, Barnes PJ, Lemiere C, et al., 2023, Developing the water paucity index using dimensional homogeneity, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-IN PRACTICE, Vol: 11, Pages: 1-8, ISSN: 2213-2198
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- Citations: 1
Bafadhel M, Faner R, Taille C, et al., 2022, Inhaled corticosteroids for the treatment of COVID-19, EUROPEAN RESPIRATORY REVIEW, Vol: 31, ISSN: 0905-9180
Casale TB, Barnes PJ, 2022, Smoke and the Lungs, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-IN PRACTICE, Vol: 10, Pages: 2852-2853, ISSN: 2213-2198
Devulder J, Baker JR, Odqvist L, et al., 2022, Extracellular vesicles propagate cellular senescence by transferring miR34a in airway epithelial cells, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Ho V, Baker JR, Willison KR, et al., 2022, An amplification-free, innovative, multiplex assay to quantify microRNAs in single cells from COPD patients, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Havaki S, Evangelou K, Paschalaki K, et al., 2022, Reply: Identification of coronavirus particles by electron microscopy: a complementary tool for deciphering COVID-19, EUROPEAN RESPIRATORY JOURNAL, Vol: 60, ISSN: 0903-1936
Havaki S, Evangelou K, Paschalaki K, et al., 2022, Reply: Identification of coronavirus particles by electron microscopy: a complementary tool for deciphering COVID-19, EUROPEAN RESPIRATORY JOURNAL, Vol: 60, ISSN: 0903-1936
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- Citations: 1
Iemoli E, Ortolani VGR, Preziosi D, et al., 2022, Failure of desensitization with Pfizer-BioNTech COVID-19 vaccine in two asthmatic patients., Eur Ann Allergy Clin Immunol, Vol: 54, Pages: 240-241, ISSN: 1764-1489
Since December 2020, in various countries of the world, many cases of severe allergic reactions after administration of PfizerBioNTech COVID-19 vaccine, were reported. A great concern has arisen among the doctors who administer the vaccine and the allergic patients who undergo vaccinations. In Italy guidelines were published in order to stratify the risk in the allergic population. In mRNA vaccines, the component currently suspected of causing allergic reactions is the polyethylene glycol excipient (PEG or macrogol). In patients who have shown an immediate allergic reaction to vaccine and who are negative to skin tests for PEG, desensitization with the same vaccine is proposed. In this paper we describe two cases of asthma after the first COVID vaccine administration in which desensitization has failed.
Baker JR, Fenwick PS, Koss CK, et al., 2022, Imbalance between IL-36 receptor agonist and antagonist drives neutrophilic inflammation in COPD, JCI Insight, Vol: 7, ISSN: 2379-3708
Current treatments fail to modify the underlying pathophysiology and disease progression of chronic obstructive pulmonary disease (COPD), necessitating alternative therapies. Here, we show that COPD subjects have increased IL-36γ and decreased IL-36 receptor antagonist (IL-36Ra) in bronchoalveolar and nasal fluid compared to control subjects. IL-36γ is derived from small airway epithelial cells (SAEC) and further induced by a viral mimetic, whereas IL-36RA is derived from macrophages. IL-36γ stimulates release of the neutrophil chemoattractants CXCL1 and CXCL8, as well as elastolytic matrix metalloproteinases (MMPs) from small airway fibroblasts (SAF). Proteases released from COPD neutrophils cleave and activate IL-36γ thereby perpetuating IL-36 inflammation. Transfer of culture media from SAEC to SAF stimulated release of CXCL1, that was inhibited by exogenous IL-36RA. The use of a therapeutic antibody that inhibits binding to the IL-36 receptor (IL-36R) attenuated IL-36γ driven inflammation and cellular cross talk. We have demonstrated a mechanism for the amplification and propagation of neutrophilic inflammation in COPD and that blocking this cytokine family via a IL-36R neutralizing antibody could be a promising new therapeutic strategy in the treatment of COPD.
Evangelou K, Veroutis D, Paschalaki K, et al., 2022, Pulmonary infection by SARS-CoV-2 induces senescence accompanied by an inflammatory phenotype in severe COVID-19: possible implications for viral mutagenesis, EUROPEAN RESPIRATORY JOURNAL, Vol: 60, ISSN: 0903-1936
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- Citations: 18
Dekhuijzen PNR, Levy ML, Corrigan CJ, et al., 2022, Is Inhaler Technique Adequately Assessed and Reported in Clinical Trials of Asthma and Chronic Obstructive Pulmonary Disease Therapy? A Systematic Review and Suggested Best Practice Checklist, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-IN PRACTICE, Vol: 10, Pages: 1813-+, ISSN: 2213-2198
Barnes PJ, 2022, Chemokine receptor CCR1: new target for asthma therapy, TRENDS IN PHARMACOLOGICAL SCIENCES, Vol: 43, Pages: 539-541, ISSN: 0165-6147
Fenwick P, Baker JR, Koss CK, et al., 2022, TRPV4 Identifies Phagocytic Macrophages and May Promote Phagocytosis in Both Healthy and COPD Cells, International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Ho V, Baker JR, Willison KR, et al., 2022, Novel Single Cell Analysis of microRNA Levels in Response to Oxidative Stress and in COPD Using Microfluidic Technology, International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Baker JR, Fenwick PS, Koss CK, et al., 2022, Inhibition of the IL-36 Receptor Reduces Viral Induced Cross-Talk Between Small Airway Epithelial Cells and Fibroblast in COPD, International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Devulder J, Baker JR, Odqvist L, et al., 2022, Transfer of microRNA Through Extracellular Vesicles Propagate Airway Epithelial Cells Senescence in COPD, International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Barnes PJ, Baker J, Donnelly LE, 2022, Autophagy in asthma and chronic obstructive pulmonary disease, CLINICAL SCIENCE, Vol: 136, Pages: 733-746, ISSN: 0143-5221
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- Citations: 5
Hassibi S, Baker JR, Barnes PJ, et al., 2022, COPD Macrophages Show Reduced Clearance of Senescent Airway Epithelial Cells, International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Wysoczanski R, Baker JR, Fenwick P, et al., 2022, Defective Phagocytosis in COPD Macrophages Is Improved by Mitochondrial Antioxidants Without Alteration in Mitochondrial Function, International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Barnes PJ, 2022, Oxidative Stress in Chronic Obstructive Pulmonary Disease, ANTIOXIDANTS, Vol: 11
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- Citations: 11
Baker JR, Mahdi M, Nicolau DV, et al., 2022, Early Th2 inflammation in the upper respiratory mucosa as a predictor of severe COVID-19 and modulation by early treatment with inhaled corticosteroids: a mechanistic analysis., The Lancet Respiratory Medicine, ISSN: 2213-2600
BACKGROUND: Community-based clinical trials of the inhaled corticosteroid budesonide in early COVID-19 have shown improved patient outcomes. We aimed to understand the inflammatory mechanism of budesonide in the treatment of early COVID-19. METHODS: The STOIC trial was a randomised, open label, parallel group, phase 2 clinical intervention trial where patients were randomly assigned (1:1) to receive usual care (as needed antipyretics were only available treatment) or inhaled budesonide at a dose of 800 μg twice a day plus usual care. For this experimental analysis, we investigated the nasal mucosal inflammatory response in patients recruited to the STOIC trial and in a cohort of SARS-CoV-2-negative healthy controls, recruited from a long-term observational data collection study at the University of Oxford. In patients with SARS-CoV-2 who entered the STOIC study, nasal epithelial lining fluid was sampled at day of randomisation (day 0) and at day 14 following randomisation, blood samples were also collected at day 28 after randomisation. Nasal epithelial lining fluid and blood samples were collected from the SARS-CoV-2 negative control cohort. Inflammatory mediators in the nasal epithelial lining fluid and blood were assessed for a range of viral response proteins, and innate and adaptive response markers using Meso Scale Discovery enzyme linked immunoassay panels. These samples were used to investigate the evolution of inflammation in the early COVID-19 disease course and assess the effect of budesonide on inflammation. FINDINGS: 146 participants were recruited in the STOIC trial (n=73 in the usual care group; n=73 in the budesonide group). 140 nasal mucosal samples were available at day 0 (randomisation) and 122 samples at day 14. At day 28, whole blood was collected from 123 participants (62 in the budesonide group and 61 in the usual care group). 20 blood or nasal samples were collected from healthy controls. In early COVID-19 disease, there was an enhanced in
Barnes PJ, 2022, INHALED THERAPIES FOR COVID-19, Publisher: MARY ANN LIEBERT, INC, Pages: A2-A2, ISSN: 1941-2711
Paschalaki K, Rossios C, Pericleous C, et al., 2022, Inhaled corticosteroids reduce senescence in endothelial progenitor cells from COPD patients, Thorax, Vol: 77, ISSN: 0040-6376
Cellular senescence contributes to the pathophysiology of chronic obstructive pulmonarydisease (COPD) and cardiovascular disease. Using endothelial-colony-forming-cells (ECFC),we have demonstrated accelerated senescence in smokers and COPD patients compared tonon-smokers. Subgroup analysis suggests that ECFC from COPD patients on inhaledcorticosteroids (ICS) (n=14; 8 on ICS) exhibited significantly reduced senescence(Senescence-associated-beta galactosidase activity, p21CIP1), markers of DNA damageresponse (DDR) and IFN-γ-inducible-protein-10 compared to COPD patients not on ICS. Invitro studies using human-umbilical-vein-endothelial-cells showed a protective effect of ICSon the DDR, senescence and apoptosis caused by oxidative-stress, suggesting a protectivemolecular mechanism of action of corticosteroids on endothelium.
Bradbury T, Di Tanna GL, Scaria A, et al., 2022, Blood Eosinophils in Chinese COPD Participants and Response to Treatment with Combination Low-Dose Theophylline and Prednisone: A Post-Hoc Analysis of the TASCS Trial, INTERNATIONAL JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE, Vol: 17, Pages: 273-282, ISSN: 1178-2005
Koss CK, Wohnhaas CT, Baker JR, et al., 2021, IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice, Communications Biology, Vol: 4, Pages: 1-15, ISSN: 2399-3642
IL-36, which belongs to the IL-1 superfamily, is increasingly linked to neutrophilic inflammation. Here, we combined in vivo and in vitro approaches using primary mouse and human cells, as well as, acute and chronic mouse models of lung inflammation to provide mechanistic insight into the intercellular signaling pathways and mechanisms through which IL-36 promotes lung inflammation. IL-36 receptor deficient mice exposed to cigarette smoke or cigarette smoke and H1N1 influenza virus had attenuated lung inflammation compared with wild-type controls. We identified neutrophils as a source of IL-36 and show that IL-36 is a key upstream amplifier of lung inflammation by promoting activation of neutrophils, macrophages and fibroblasts through cooperation with GM-CSF and the viral mimic poly(I:C). Our data implicate IL-36, independent of other IL-1 family members, as a key upstream amplifier of neutrophilic lung inflammation, providing a rationale for targeting IL-36 to improve treatment of a variety of neutrophilic lung diseases.
Bateman ED, O'Byrne PM, FitzGerald JM, et al., 2021, Positioning As-needed Budesonide-Formoterol for Mild Asthma Effect of Prestudy Treatment in Pooled Analysis of SYGMA 1 and 2, ANNALS OF THE AMERICAN THORACIC SOCIETY, Vol: 18, Pages: 2007-2017, ISSN: 1546-3222
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- Citations: 4
Adeloye D, Elneima O, Daines L, et al., 2021, The long-term sequelae of COVID-19: an international consensus on research priorities for patients with pre-existing and new-onset airways disease, LANCET RESPIRATORY MEDICINE, Vol: 9, Pages: 1467-1478, ISSN: 2213-2600
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- Citations: 42
Reddel HK, O'Byrne PM, FitzGerald JM, et al., 2021, Reply to "As-needed budesonideformoterol for adolescents with mild asthma: importance of lung function'', JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY-IN PRACTICE, Vol: 9, Pages: 4179-4180, ISSN: 2213-2198
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