Imperial College London

Professor Peter Barnes, FRS

Faculty of MedicineNational Heart & Lung Institute

Senior Research Investigator
 
 
 
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Contact

 

+44 (0)20 7594 7959p.j.barnes Website

 
 
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Assistant

 

Miss Carolyn Green +44 (0)20 7594 7959

 
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Location

 

227CGuy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Publication Type
Year
to

2385 results found

Casale TB, Barnes PJ, 2022, Smoke and the Lungs., J Allergy Clin Immunol Pract, Vol: 10, Pages: 2852-2853

Journal article

Pavord ID, Barnes PJ, Lemiere C, Gibson PGet al., 2022, Diagnosis and assessment of the asthmas., J Allergy Clin Immunol Pract

Optimising asthma diagnosis is an essential part of global strategies to reduce the excessive illness burden from asthma. New understanding about how to address the complexity and heterogeneity of the different forms of asthma mean that asthma diagnosis now requires a compound diagnostic approach and label. Eliciting the typical symptoms and abnormal physiology of variable airflow limitation permit the recognition of asthma, and the identification of further features, such as eosinophilic or type-2 inflammation, allow a compound diagnostic label of eosinophilic asthma. This conveys key information about future exacerbation risk and likely treatment responsiveness. Treatable traits is a useful way to implement this new approach to diagnosis. Targeted assessment is used to inform a specific treatment plan in a pragmatic and iterative process.

Journal article

Havaki S, Evangelou K, Paschalaki K, Petty R, Barnes PJ, Gorgoulis VGet 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

Journal article

Iemoli E, Ortolani VGR, Preziosi D, Caron L, Giardina C, Carlevatti V, Giovine Net 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.

Journal article

Baker JR, Fenwick PS, Koss CK, Owles HB, Elkin SL, Fine JS, Thomas M, Kasmi KC, Barnes PJ, Donnelly LEet 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.

Journal article

Dekhuijzen PNR, Levy ML, Corrigan CJ, Hadfield RM, Roche N, Usmani OS, Barnes PJ, Scullion JE, Lavorini F, Corbetta L, Kocks JWH, Cosio BG, Buhl R, Pedersen SEet 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

Journal article

Barnes PJ, 2022, Chemokine receptor CCR1: new target for asthma therapy, TRENDS IN PHARMACOLOGICAL SCIENCES, Vol: 43, Pages: 539-541, ISSN: 0165-6147

Journal article

Devulder J, Baker JR, Odqvist L, Donnelly LE, Barnes PJet al., 2022, Transfer of microRNA Through Extracellular Vesicles Propagate Airway Epithelial Cells Senescence in COPD, Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Baker JR, Fenwick PS, Koss CK, Owles HB, El Kasmi KC, Barnes PJ, Donnelly LEet al., 2022, Inhibition of the IL-36 Receptor Reduces Viral Induced Cross-Talk Between Small Airway Epithelial Cells and Fibroblast in COPD, Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Ho V, Baker JR, Willison KR, Klug DR, Barnes PJ, Donnelly LEet al., 2022, Novel Single Cell Analysis of microRNA Levels in Response to Oxidative Stress and in COPD Using Microfluidic Technology, Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Fenwick P, Baker JR, Koss CK, Ramirez F, Barnes PJ, El Kasmi KC, Donnelly LEet al., 2022, TRPV4 Identifies Phagocytic Macrophages and May Promote Phagocytosis in Both Healthy and COPD Cells, Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Wysoczanski R, Baker JR, Fenwick P, Alexandrov Y, Dunsby C, French P, Barnes PJ, Donnelly LEet al., 2022, Defective Phagocytosis in COPD Macrophages Is Improved by Mitochondrial Antioxidants Without Alteration in Mitochondrial Function, Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

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

Journal article

Barnes PJ, 2022, Oxidative Stress in Chronic Obstructive Pulmonary Disease, ANTIOXIDANTS, Vol: 11

Journal article

Hassibi S, Baker JR, Barnes PJ, Donnelly LEet al., 2022, COPD Macrophages Show Reduced Clearance of Senescent Airway Epithelial Cells, Publisher: AMER THORACIC SOC, ISSN: 1073-449X

Conference paper

Havaki S, Evangelou K, Paschalaki K, Petty R, Barnes PJ, Gorgoulis VGet al., 2022, Identification of coronavirus particles by electron microscopy: a complementary tool for deciphering COVID-19., Eur Respir J

Journal article

Baker JR, Mahdi M, Nicolau DV, Ramakrishnan S, Barnes PJ, Simpson JL, Cass SP, Russell REK, Donnelly LE, Bafadhel Met 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

Journal article

Barnes PJ, 2022, INHALED THERAPIES FOR COVID-19, Publisher: MARY ANN LIEBERT, INC, Pages: A2-A2, ISSN: 1941-2711

Conference paper

Paschalaki K, Rossios C, Pericleous C, MacLeod M, Rothery S, Donaldson G, Wedzicha J, Gorgoulis V, Randi A, Barnes Pet 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.

Journal article

Bradbury T, Di Tanna GL, Scaria A, Martin A, Wen F-Q, Zhong N-S, Zheng J-P, Barnes PJ, Celli B, Berend N, Jenkins CRet 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

Journal article

Koss CK, Wohnhaas CT, Baker JR, Tilp C, Przibilla M, Lerner C, Frey S, Keck M, Williams CMM, Peter D, Ramanujam M, Fine J, Gantner F, Thomas M, Barnes PJ, Donnelly LE, El Kasmi KCet 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.

Journal article

Bateman ED, O'Byrne PM, FitzGerald JM, Barnes PJ, Zheng J, Lamarca R, Puu M, Parikh H, Alagappan V, Reddel HKet 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

Journal article

Adeloye D, Elneima O, Daines L, Poinasamy K, Quint JK, Walker S, Brightling CE, Siddiqui S, Hurst JR, Chalmers JD, Pfeffer PE, Novotny P, Drake TM, Heaney LG, Rudan I, Sheikh A, De Soyza Aet 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

Journal article

Reddel HK, O'Byrne PM, FitzGerald JM, Barnes PJ, Zheng J, Ivanov S, Lamarca R, Puu M, Alagappan VKT, Bateman EDet 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

Journal article

Baker JR, Fenwick PS, Owles HB, Koss C, El-Kasmi K, Barnes PJ, Donnelly LEet al., 2021, IL-36? - a key mediator of neutrophilic inflammation in chronic obstructive pulmonary disease, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Devulder J, Baker JR, Donnelly LE, Barnes PJet al., 2021, Extracellular vesicles produced by airway epithelial cells in response to oxidative stress contain microRNAs associated with cellular senescence, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Yu L-M, Bafadhel M, Dorward J, Hayward G, Saville BR, Gbinigie O, Van Hecke O, Ogburn E, Evans PH, Thomas NPB, Patel MG, Richards D, Berry N, Detry MA, Saunders C, Fitzgerald M, Harris V, Shanyinde M, De Lusignan S, Andersson MI, Barnes PJ, Russell REK, Nicolau DV, Ramakrishnan S, Hobbs FDR, Butler CCet al., 2021, Inhaled budesonide for COVID-19 in people at high risk of complications in the community in the UK (PRINCIPLE): a randomised, controlled, open-label, adaptive platform trial, LANCET, Vol: 398, Pages: 843-855, ISSN: 0140-6736

Journal article

Reddel HK, O'Byrne PM, FitzGerald JM, Barnes PJ, Zheng J, Ivanov S, Lamarca R, Puu M, Alagappan VKT, Bateman EDet al., 2021, Efficacy and Safety of As-Needed Budesonide-Formoterol in Adolescents with Mild Asthma, International Conference of the American-Thoracic-Society, Publisher: ELSEVIER, Pages: 3069-+, ISSN: 2213-2198

Conference paper

Norwitz NG, Winwood R, Stubbs BJ, D'Agostino DP, Barnes PJet al., 2021, Case Report: Ketogenic Diet Is Associated With Improvements in Chronic Obstructive Pulmonary Disease, FRONTIERS IN MEDICINE, Vol: 8

Journal article

Ramakrishnan S, Nicolau D, Langford B, Mahdi M, Jeffers H, Mwasuku C, Krassowska K, Fox R, Binnian I, Glover V, Bright S, Butler C, Cane J, Halner A, Matthews P, Donnelly L, Simpson J, Baker J, Fadai N, Peterson S, Bengtsson T, Barnes P, Russell R, Bafadhel Met al., 2021, Inhaled budesonide in the treatment of early COVID-19 (STOIC): a phase 2, open-label, randomised controlled trial, LANCET RESPIRATORY MEDICINE, Vol: 9, Pages: 763-772, ISSN: 2213-2600

Journal article

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