Publications
2499 results found
Fukuda Y, Akimoto K, Homma T, et al., 2020, Virus-Induced Asthma Exacerbations: SIRT1 Targeted Approach, JOURNAL OF CLINICAL MEDICINE, Vol: 9
- Author Web Link
- Cite
- Citations: 8
Scichilone N, Barnes PJ, Battaglia S, et al., 2020, The Hidden Burden of Severe Asthma: From Patient Perspective to New Opportunities for Clinicians, JOURNAL OF CLINICAL MEDICINE, Vol: 9
- Author Web Link
- Cite
- Citations: 3
Baker JR, Donnelly LE, Barnes PJ, 2020, Senotherapy A New Horizon for COPD Therapy, CHEST, Vol: 158, Pages: 562-570, ISSN: 0012-3692
- Author Web Link
- Cite
- Citations: 31
Siddharthan T, Gupte A, Barnes PJ, 2020, Chronic Obstructive Pulmonary Disease Endotypes in Low- and Middle-Income Country Settings: Precision Medicine for All, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 202, Pages: 171-172, ISSN: 1073-449X
- Author Web Link
- Cite
- Citations: 11
Papadopoulos NG, Barnes P, Canonica GW, et al., 2020, The evolving algorithm of biological selection in severe asthma, ALLERGY, Vol: 75, Pages: 1555-1563, ISSN: 0105-4538
- Author Web Link
- Cite
- Citations: 24
FitzGerald JM, Barnes PJ, Chipps BE, et al., 2020, The burden of exacerbations in mild asthma: a systematic review, ERJ OPEN RESEARCH, Vol: 6
- Author Web Link
- Cite
- Citations: 29
Barnes PJ, 2020, Oxidative stress-based therapeutics in COPD, REDOX BIOLOGY, Vol: 33, ISSN: 2213-2317
- Author Web Link
- Cite
- Citations: 150
Usmani OS, Matthews JC, Wright MD, et al., 2020, No evidence electric charge increases inhaled ultrafine particle deposition in human lungs, American Journal of Respiratory and Critical Care Medicine, Vol: 201, Pages: 1301-1303, ISSN: 1073-449X
Salvi SS, Brashier BB, Londhe J, et al., 2020, Phenotypic comparison between smoking and non-smoking chronic obstructive pulmonary disease, RESPIRATORY RESEARCH, Vol: 21
- Author Web Link
- Cite
- Citations: 39
Paredi P, Barnes P, 2020, The Application of Analytical Technique Applied to Expired Air as a Means of Monitoring Airway and Lung Function, Cotes’ Lung Function, Seventh Edition, Pages: 129-147, ISBN: 9781118597323
Inflammation is a non-specific reaction of vascularised tissues to injury. Accurate assessment of inflammation in the lung is important in the clinical management of pulmonary diseases and may allow the clinician to monitor their progression and to establish the efficacy of anti-inflammatory or anti-oxidant treatment. However monitoring inflammation is difficult and may not be reflected in conventional lung function tests or by monitoring changes in haematological markers. There has been great interest in the measurement of nitric oxide (NO) and other exhaled markers of oxidative stress and inflammation. In addition, exhaled ethane has been suggested as a marker of lipid peroxidation, whereas exhaled breath temperature (Δe T) and bronchial blood flow may reflect inflammation and two of its cardinal signs, rubor (redness) and calor (heat). In this chapter, we describe the measurement of exhaled NO, but we will also discuss volatile organic compounds, exhaled breath temperature, and bronchial blood flow as a complement to measurement of exhaled NO.
Gorlitz F, Wysoczanski R, Kumar S, et al., 2020, Towards easier, faster super-resolved microscopy, Conference on Single Molecule Spectroscopy and Superresolution Imaging XIII, Publisher: SPIE-INT SOC OPTICAL ENGINEERING, ISSN: 0277-786X
Wrench CL, Baker JR, Fenwick PS, et al., 2020, Alterations in Antioxidant Expression with Oxidative Stress in Small Airway Fibroblasts from COPD Patients, Virtual International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Devulder J, Baker J, Donnelly L, et al., 2020, Extracellular Vesicles Produced by Bronchial Epithelial Cells in Response to Oxidative Stress Contain Micro-RNAs Associated with Cellular Senescence, Virtual International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Baker J, Fenwick PS, Donnelly LE, et al., 2020, Elevated Levels of Cellular Senescence and Senescence-Associated Secretory Phenotype Markers in COPD Small Airway Epithelial Cells, Virtual International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Mercado N, Colley T, Baker JR, et al., 2019, Bicaudal D1 impairs autophagosome maturation in chronic obstructive pulmonary disease, FASEB BIOADVANCES, Vol: 1, Pages: 688-705
- Author Web Link
- Cite
- Citations: 10
Barnes PJ, Szefler SJ, Reddel HK, et al., 2019, Symptoms and perception of airway obstruction in asthmatic patients: Clinical implications for use of reliever medications, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 144, Pages: 1180-1186, ISSN: 0091-6749
- Author Web Link
- Cite
- Citations: 39
Barnes PJ, 2019, Small airway fibrosis in COPD, INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, Vol: 116, ISSN: 1357-2725
- Author Web Link
- Cite
- Citations: 45
Belchamber K, Singh R, Batista C, et al., 2019, Defective bacterial phagocytosis is associated with dysfunctional mitochondria in COPD macrophages, European Respiratory Journal, Vol: 54, Pages: 1-14, ISSN: 0903-1936
Background: Increased reactive oxygen species (ROS) have been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). Objective: This study examined the effect of exogenous and endogenous oxidative stress on macrophage phagocytosis in patients with COPD. Methods: Monocyte-derived macrophages (MDM) were generated from non-smoker, smoker and COPD subjects, differentiated in either GM-CSF (G-Mϕ) or M-CSF (M-Mϕ). Alveolar macrophages were isolated from lung tissue or bronchoalveolar lavage. Macrophages were incubated +/- 200M H2O2 for 24 hours, then exposed to fluorescently-labelled H. influenzae or S. pneumoniae for 4 hours, after which phagocytosis, mitochondrial ROS (mROS), and mitochondrial membrane potential (m) were measured. Results: Phagocytosis of bacteria was significantly decreased in both G-Mϕ and M-Mϕ from COPD patients, compared to non-smoker controls. In non-smokers and smokers, bacterial phagocytosis did not alter mROS or m, however in COPD, phagocytosis increased early mROS and decreased m in both G-Mϕ and M-Mϕ. Exogenous oxidative stress reduced phagocytosis in non-smoker and COPD alveolar macrophages, and non-smoker MDM, associated with reduced mROS production. Conclusion: COPD macrophages show defective phagocytosis, which is associated with altered mitochondrial function and an inability to regulate mROS production. Targeting mitochondrial dysfunction may restore the phagocytic defect in COPD.
Barnes PJ, 2019, Nitrosative stress in patients with asthma-chronic obstructive pulmonary disease overlap, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 144, Pages: 928-930, ISSN: 0091-6749
- Author Web Link
- Cite
- Citations: 5
Wrench C, Baker J, Fenwick P, et al., 2019, COPD Small Airway Fibroblasts show reduced proliferation rate and are arrested in G1 phase, International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Hassibi S, Baker J, Donnelly L, et al., 2019, The RNA binding protein HuR regulates the senescence-associated secretory phenotype under conditions of oxidative stress, International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
- Author Web Link
- Cite
- Citations: 3
Reddel H, Bateman ED, Fitzgerald JM, et al., 2019, Exacerbation risk after night-time waking due to asthma in SYGMA 1, International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
- Author Web Link
- Cite
- Citations: 2
Fitzgerald M, O'Byrne PM, Bateman ED, et al., 2019, Number needed to treat (NNT) to have an additional patient free from a severe or moderate/severe exacerbation: post-hoc analysis of SYGMA 1 in mild asthma, International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
- Author Web Link
- Cite
- Citations: 2
Anders KL, Belchamber KBR, Barnes PJ, et al., 2019, Differential phosphorylation patterns of macrophage cytoskeletal proteins in COPD following phagocytosis, International Congress of the European-Respiratory-Society (ERS), Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Barnes PJ, Baker J, Donnelly LE, 2019, Cellular senescence as a mechanism and target in chronic lung diseases, American Journal of Respiratory and Critical Care Medicine, Vol: 200, ISSN: 1073-449X
Cellular senescence is now considered an important driving mechanism for chronic lung diseases, particularly COPD and idiopathic pulmonary fibrosis. Cellular senescence is due to replicative and stress-related senescence with activation of p53 and p16INK4a respectively, leading to activation of p21CIP1 and cell cycle arrest. Senescent cells secrete multiple inflammatory proteins known as the senescence-associated secretory phenotype (SASP), leading to low grade chronic inflammation, which further drives senescence. Loss of key anti-aging molecules sirtuin-1 and sirtuin-6 may be important in acceleration of aging and arises from oxidative stress reducing phosphatase PTEN, thereby activating PI3K (phosphoinositide-3-kinase) and mTOR (mammalian target of rapamycin). MicroRNA-34a, which is regulated by PI3K-mTOR signaling, plays a pivotal role in reducing sirtuin-1/6 and its inhibition with an antagomir results in their restoration, reducing markers of senescence, reducing SASP and reversing cell cycle arrest in epithelial cells from peripheral airways of COPD patients. MiR-570 is also involved in reduction of sirtuin-1 and cellular senescence and is activated by p38 MAP kinase. These miRNAs may be released from cells in extracellular vesicles that are taken up by other cells, thereby spreading senescence locally within the lung but outside the lung through the circulation; this may account for comorbidities of COPD and other lung diseases. Understanding the mechanisms of cellular senescence may result in new treatments for chronic lung disease, either by inhibiting PI3K-mTOR signaling, by inhibiting specific miRNAs or by deletion of senescent cells with senolytic therapies, already shown to be effective in experimental lung fibrosis.
Roche N, Anzueto A, Anticevich SB, et al., 2019, The importance of real-life research in respiratory medicine: manifesto of the Respiratory Effectiveness Group, European Respiratory Journal, Vol: 54, Pages: 1-6, ISSN: 0903-1936
Efthimiou J, Poll C, Barnes PJ, 2019, Dual mechanism of action of T2 inhibitor therapies in virally induced exacerbations of asthma: evidence for a beneficial counter-regulation, EUROPEAN RESPIRATORY JOURNAL, Vol: 54, ISSN: 0903-1936
- Author Web Link
- Cite
- Citations: 10
Devereux G, Cotton S, Fielding S, et al., 2019, Introduction, HEALTH TECHNOLOGY ASSESSMENT, Vol: 23, Pages: 1-+, ISSN: 1366-5278
- Author Web Link
- Cite
- Citations: 5
Leaker BR, Singh D, Nicholson GC, et al., 2019, Evaluation of systemic absorption and bronchodilator effect of glycopyrronium bromide delivered by nebulizer or a dry powder inhaler in subjects with chronic obstructive pulmonary disease, RESPIRATORY RESEARCH, Vol: 20
- Author Web Link
- Cite
- Citations: 4
Singh D, Agusti A, Anzueto A, et 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.
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.