Imperial College London

Professor Sir Peter Barnes, FRS, FMedSci

Faculty of MedicineNational Heart & Lung Institute

Senior Research Investigator
 
 
 
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Contact

 

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

 
 
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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

2498 results found

Wrench CL, Baker JR, Monkley S, Fenwick PS, Murray L, Donnelly LE, Barnes PJet al., 2024, Small airway fibroblasts from patients with chronic obstructive pulmonary disease exhibit cellular senescence., Am J Physiol Lung Cell Mol Physiol, Vol: 326, Pages: L266-L279

Small airway disease (SAD) is a key early-stage pathology of chronic obstructive pulmonary disease (COPD). COPD is associated with cellular senescence whereby cells undergo growth arrest and express the senescence-associated secretory phenotype (SASP) leading to chronic inflammation and tissue remodeling. Parenchymal-derived fibroblasts have been shown to display senescent properties in COPD, however small airway fibroblasts (SAFs) have not been investigated. Therefore, this study investigated the role of these cells in COPD and their potential contribution to SAD. To investigate the senescent and fibrotic phenotype of SAF in COPD, SAFs were isolated from nonsmoker, smoker, and COPD lung resection tissue (n = 9-17 donors). Senescence and fibrotic marker expressions were determined using iCELLigence (proliferation), qPCR, Seahorse assay, and ELISAs. COPD SAFs were further enriched for senescent cells using FACSAria Fusion based on cell size and autofluorescence (10% largest/autofluorescent vs. 10% smallest/nonautofluorescent). The phenotype of the senescence-enriched population was investigated using RNA sequencing and pathway analysis. Markers of senescence were observed in COPD SAFs, including senescence-associated β-galactosidase, SASP release, and reduced proliferation. Because the pathways driving this phenotype were unclear, we used cell sorting to enrich senescent COPD SAFs. This population displayed increased p21CIP1 and p16INK4a expression and mitochondrial dysfunction. RNA sequencing suggested these senescent cells express genes involved in oxidative stress response, fibrosis, and mitochondrial dysfunction pathways. These data suggest COPD SAFs are senescent and may be associated with fibrotic properties and mitochondrial dysfunction. Further understanding of cellular senescence in SAFs may lead to potential therapies to limit SAD progression.NEW & NOTEWORTHY Fibroblasts and senescence are thought to play key roles in the pathogenesis of small airw

Journal article

Levy ML, Beasley R, Bostock B, Capstick TG, Crooks MG, Fleming L, Freeman D, Marsh V, Rupani H, Whittamore A, Barnes PJ, Bush Aet al., 2024, A simple and effective evidence-based approach to asthma management: ICS-formoterol reliever therapy., Br J Gen Pract, Vol: 74, Pages: 86-89

Journal article

Ariel A, Barnes PJ, Maricoto T, Román-Rodríguez M, Powell A, Quint JKet al., 2023, Rational use of inhaled corticosteroids for the treatment of COPD: a plain language summary., J Comp Eff Res, Vol: 12

WHAT IS THIS SUMMARY ABOUT?: Inhaled corticosteroids (ICS) are a type of medication delivered via an inhaler device that are commonly used in the treatment of asthma. ICS can also be used to treat chronic obstructive pulmonary disease (COPD), a progressive respiratory condition in which the lungs become worse over time. However, unlike in asthma, ICS are only effective in a small proportion of people with COPD. ICS can cause significant side effects in people with COPD, including pneumonia. Because of this, guidelines written by COPD experts recommend that ICS should largely be prescribed to people with COPD whose symptoms flare up frequently and become difficult to manage (episodes known as exacerbations). Despite this guidance, records collected from routine clinical practice suggest that many healthcare professionals prescribe ICS to people with COPD who do not have frequent exacerbations, putting them at unnecessary risk of side effects. The over-prescription of ICS in COPD may partly be due to the recent introduction of single-inhaler combination therapies, which combine ICS with other medicines (bronchodilators). This 'one inhaler for all' approach is a concerning trend as it goes against global COPD treatment guidelines, which recommend ICS use in only a small proportion of people. This is a plain language summary of a review article originally published in the journal NPJ Primary Care Respiratory Medicine. In this review, we investigate the benefits and risks of ICS use in COPD. Using data from both randomized controlled trials (RCTs) and observational studies, we explain which people benefit from ICS use, and why health regulatory bodies have concluded that ICS do not help people with COPD to live longer. Lastly, we provide practical guidance for doctors and people with COPD regarding when ICS should be prescribed and when they should be withdrawn.

Journal article

Chiarella SE, Barnes PJ, 2023, Endogenous inhibitory mechanisms in asthma., J Allergy Clin Immunol Glob, Vol: 2

Endogenous inhibitory mechanisms promote resolution of inflammation, enhance tissue repair and integrity, and promote homeostasis in the lung. These mechanisms include steroid hormones, regulatory T cells, IL-10, prostaglandin E2, prostaglandin I2, lipoxins, resolvins, protectins, maresins, glucagon-like peptide-1 receptor, adrenomedullin, nitric oxide, and carbon monoxide. Here we review the most recent literature regarding these endogenous inhibitory mechanisms in asthma, which remain a promising target for the prevention and treatment of asthma.

Journal article

Jia M, Fu H, Jiang X, Wang L, Xu J, Barnes PJ, Adcock IM, Liu Y, He S, Zhang F, Yao L, Sun P, Yao Xet al., 2023, DEL-1, as an anti-neutrophil transepithelial migration molecule, inhibits airway neutrophilic inflammation in asthma., Allergy

BACKGROUND: Neutrophil migration into the airways is a key process in neutrophilic asthma. Developmental endothelial locus-1 (DEL-1), an extracellular matrix protein, is a neutrophil adhesion inhibitor that attenuates neutrophilic inflammation. METHODS: Levels of DEL-1 were measured in exhaled breath condensate (EBC) and serum in asthma patients by ELISA. DEL-1 modulation of neutrophil adhesion and transepithelial migration was examined in a co-culture model in vitro. The effects of DEL-1-adenoviral vector-mediated overexpression on ovalbumin/lipopolysaccharide (OVA/LPS)-induced neutrophilic asthma were studied in mice in vivo. RESULTS: DEL-1 was primarily expressed in human bronchial epithelial cells and was decreased in asthma patients. Serum DEL-1 concentrations were reduced in patients with severe asthma compared with normal subjects (567.1 ± 75.3 vs. 276.8 ± 29.36 pg/mL, p < .001) and were negatively correlated to blood neutrophils (r = -0.2881, p = .0384) and neutrophil-to-lymphocyte ratio (NLR) (r = -0.5469, p < .0001). DEL-1 concentrations in the EBC of severe asthmatic patients (113.2 ± 8.09 pg/mL) were also lower than normal subjects (193.0 ± 7.61 pg/mL, p < .001) and were positively correlated with the asthma control test (ACT) score (r = 0.3678, p = .0035) and negatively related to EBC IL-17 (r = -0.3756, p = .0131), myeloperoxidase (MPO) (r = -0.5967, p = .0055), and neutrophil elastase (NE) (r = -0.5488, p = .0009) expression in asthma patients. Neutrophil adhesion and transepithelial migration in asthma patients were associated with LFA-1 binding to ICAM-1 and inhibited by DEL-1. DEL-1 mRNA and protein expression in human bronchial epithelial cell

Journal article

Cazzola M, Rogliani P, Barnes PJ, Blasi F, Celli B, Hanania NA, Martinez FJ, Miller BE, Miravitlles M, Page CP, Tal-Singer R, Matera MGet al., 2023, An Update on Outcomes for COPD Pharmacological Trials: A COPD Investigators Report - Reassessment of the 2008 American Thoracic Society/European Respiratory Society Statement on Outcomes for COPD Pharmacological Trials, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 208, Pages: 374-394, ISSN: 1073-449X

Journal article

Quint JK, Ariel A, Barnes PJ, 2023, Rational use of inhaled corticosteroids for the treatment of COPD, NPJ PRIMARY CARE RESPIRATORY MEDICINE, Vol: 33

Journal article

Sin DD, Doiron D, Agusti A, Anzueto A, Barnes PJ, Celli BR, Criner GJ, Halpin D, Han MK, Martinez FJ, Oca MMD, Papi A, Pavord I, Roche N, Singh D, Stockley R, Varlera VL, Wedzicha J, Vogelmeier C, Bourbeau J, GOLD SCet al., 2023, Air pollution and COPD: GOLD 2023 committee report, EUROPEAN RESPIRATORY JOURNAL, Vol: 61, ISSN: 0903-1936

Journal article

Ho V, Baker J, Willison K, Barnes P, Donnelly L, Klug Det al., 2023, Single cell quantification of microRNA from small numbers of non-invasively sampled primary human cells, Communications Biology, Vol: 6, Pages: 1-11, ISSN: 2399-3642

Expression levels of microRNAs (miRNAs) in single cells are low and conventional miRNA detection methods require amplification that can be complex, time-consuming, costly and may bias results. Single cell microfluidic platforms have been developed; however, current approaches are unable to absolutely quantify single miRNA molecules expressed in single cells. Herein, we present an amplification-free sandwich hybridisation assay to detect single miRNA molecules in single cells using a microfluidic platform that optically traps and lyses individual cells. Absolute quantification of miR-21 and miR-34a molecules was achieved at a single cell level in human cell lines and validated using real-time qPCR. The sensitivity of the assay was demonstrated by quantifying single miRNA molecules in nasal epithelial cells and CD3+ T-cells, as well as nasal fluid collected non-invasively from healthy individuals. This platform requires ~50 cells or ~30 µL biofluid and can be extended for other miRNA targets therefore it could monitor miRNA levels in disease progression or clinical studies.

Journal article

Agusti A, Celli BR, Criner GJ, Halpin D, Anzueto A, Barnes P, Bourbeau J, Han MK, Martinez FJ, de Oca MM, Mortimer K, Papi A, Pavord I, Roche N, Salvi S, Sin DD, Singh D, Stockley R, Varela MVL, Wedzicha JA, Vogelmeier CFet al., 2023, Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary, EUROPEAN RESPIRATORY JOURNAL, Vol: 61, ISSN: 0903-1936

Journal article

Agusti A, Celli BR, Criner GJ, Halpin D, Anzueto A, Barnes P, Bourbeau J, Han MK, Martinez FJ, de Oca MM, Mortimer K, Papi A, Pavord I, Roche N, Salvi S, Sin DD, Singh D, Stockley R, Varela MVL, Wedzicha JA, Vogelmeier CF, Agusti A, Celli BR, Criner GJ, Halpin D, Anzueto A, Barnes P, Bourbeau J, Han MK, Martinez FJ, de Oca MM, Mortimer K, Papi A, Pavord I, Roche N, Salvi S, Sin DD, Singh D, Stockley R, Varela MVL, Wedzicha JA, Vogelmeier CFet al., 2023, Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary, RESPIROLOGY, Vol: 28, Pages: 316-338, ISSN: 1323-7799

Journal article

Agustí A, Celli BR, Criner GJ, Halpin D, Anzueto A, Barnes P, Bourbeau J, Han MK, Martinez FJ, Montes de Oca M, Mortimer K, Papi A, Pavord I, Roche N, Salvi S, Sin DD, Singh D, Stockley R, López Varela MV, Wedzicha JA, Vogelmeier CFet al., 2023, Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary., Am J Respir Crit Care Med, Vol: 207, Pages: 819-837

Journal article

Agusti A, Celli BR, Criner GJ, Halpin D, Anzueto A, Barnes P, Bourbeau J, Han MK, Martinez FJ, de Oca MM, Mortimer K, Papi A, Pavord I, Roche N, Salvi S, Sin DD, Singh D, Stockley R, Lopez Varela V, Wedzicha JA, Vogelmeier CFet al., 2023, Global Initiative for Chronic Obstructive Lung Disease 2023 Report: GOLD Executive Summary, ARCHIVOS DE BRONCONEUMOLOGIA, Vol: 59, Pages: 232-248, ISSN: 0300-2896

Journal article

Ombredane HCJ, Fenwick PS, Barnes PJ, Bafadhel M, Ito K, Donnelly LE, Baker JRet al., 2023, Temporal Release of IL-1 Family Members from Virally Infected Airway Epithelial Cells Suggests IL-36γ Is the Early Responder, AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, Vol: 68, Pages: 339-341, ISSN: 1044-1549

Journal article

Ahmad S, Noor NM, Syafirah EAREN, Irekeola AA, Shueb RH, Chan YY, Barnes PJ, Mohamud Ret al., 2023, Anti-Tumor Necrosis Factor for Supplementary Management in Severe Asthma: A Systematic Review and Meta-analysis, JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, Vol: 43, Pages: 77-85, ISSN: 1079-9907

Journal article

Barnes PJ, Godfrey S, 2023, Chronic obstrudive pulmonary disease, Second Edition, ISBN: 9781003420316

This book provides an up-to-date perspective on the inflammatory cells, mediators, and molecular pathology of Chronic obstructive pulmonary disease (COPD), emphasizing the urgent need to clearly understand the underlying cellular and molecular mechanisms involved in COPD.

Book

Batista C, Singer DRJ, Barnes PJ, 2023, Pocket Prescriber Pulmonary Medicine, ISBN: 9781498744409

Pocket Prescriber Pulmonary Medicine is a concise, up-to-date prescribing guide containing all the ‘must-have’ information that clinical professionals treating patients with respiratory conditions need to know. This book provides focused information for all health professionals prescribing drugs for or to patients with a respiratory condition and is an essential guide for pulmonologists, intensive care physicians, emergency medicine doctors and general practitioners and nurse prescribers, in training and in practice.

Book

Pavord ID, Barnes PJ, Lemiere C, Gibson PGet 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

Journal article

Barnes PJ, 2023, Senotherapy for lung diseases., Pages: 249-271

Increasing evidence suggests that there is acceleration of lung ageing in chronic lung diseases, such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), with the accumulation of senescent cells in the lung. Senescent cells fail to repair tissue damage and release an array of inflammatory proteins, known as the senescence-associated secretory phenotype, which drive further senescence and disease progression. This suggests that targeting cellular senescence with senotherapies may treat the underlying disease process in COPD and IPF and thus reduce disease progression and mortality. Several existing or future drugs may inhibit the development of cellular senescence which is driven by chronic oxidative stress (senostatics), including inhibitors of PI3K-mTOR signalling pathways, antagomirs of critical microRNAs and novel antioxidants. Other drugs (senolytics) selectively remove senescent cells by promoting apoptosis. Clinical studies with senotherapies are already underway in chronic lung diseases.

Book chapter

Bafadhel M, Faner R, Taille C, Russell REK, Welte T, Barnes PJ, Agusti Aet al., 2022, Inhaled corticosteroids for the treatment of COVID-19, EUROPEAN RESPIRATORY REVIEW, Vol: 31, ISSN: 0905-9180

Journal article

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

Journal article

Ho V, Baker JR, Willison KR, Klug DR, Barnes PJ, Donnelly LEet 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

Conference paper

Devulder J, Baker JR, Odqvist L, Donnelly LE, Barnes PJet al., 2022, Extracellular vesicles propagate cellular senescence by transferring miR34a in airway epithelial cells, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

Hassibi S, Baker J, Barnes P, Donnelly Let al., 2022, COPD Monocyte-derived macrophages display hallmarks of senescence, Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936

Conference paper

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

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

Evangelou K, Veroutis D, Paschalaki K, Foukas PG, Lagopati N, Dimitriou M, Papaspyropoulos A, Konda B, Hazapis O, Polyzou A, Havaki S, Kotsinas A, Kittas C, Tzioufas AG, De Leval L, Vassilakos D, Tsiodras S, Stripp BR, Papantonis A, Blandino G, Karakasiliotis I, Barnes PJ, Gorgoulis VG, Evangelou K, Veroutis D, Paschalaki K, Foukas PG, Lagopati N, Dimitriou M, Papaspyropoulos A, Konda B, Hazapis O, Polyzou A, Havaki S, Kotsinas A, Kittas C, Tzioufas AG, de Leval L, Vassilakos D, Tsiodras S, Stripp BR, Papantonis A, Blandino G, Karakasiliotis I, Barnes PJ, Gorgoulis VGet 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

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

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