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Search Results: 1 - 10 of 324111 matches for " Peter J Barnes "
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A Blood Test for Lung Fibrosis
Peter J Barnes
PLOS Medicine , 2008, DOI: 10.1371/journal.pmed.0050098
Abstract:
Chronic Obstructive Pulmonary Disease: A Growing but Neglected Global Epidemic
Peter J Barnes
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040112
Abstract:
Chronic Obstructive Pulmonary Disease: Effects beyond the Lungs
Peter J. Barnes
PLOS Medicine , 2010, DOI: 10.1371/journal.pmed.1000220
Abstract:
Inhaled Corticosteroids
Peter J. Barnes
Pharmaceuticals , 2010, DOI: 10.3390/ph3030514
Abstract: Inhaled corticosteroids (ICS) are the most effective controllers of asthma. They suppress inflammation mainly by switching off multiple activated inflammatory genes through reversing histone acetylation via the recruitment of histone deacetylase 2 (HDAC2). Through suppression of airway inflammation ICS reduce airway hyperresponsiveness and control asthma symptoms. ICS are now first-line therapy for all patients with persistent asthma, controlling asthma symptoms and preventing exacerbations. Inhaled long-acting β 2-agonists added to ICS further improve asthma control and are commonly given as combination inhalers, which improve compliance and control asthma at lower doses of corticosteroids. By contrast, ICS provide much less clinical benefit in COPD and the inflammation is resistant to the action of corticosteroids. This appears to be due to a reduction in HDAC2 activity and expression as a result of oxidative stress. ICS are added to bronchodilators in patients with severe COPD to reduce exacerbations. ICS, which are absorbed from the lungs into the systemic circulation, have negligible systemic side effects at the doses most patients require, although the high doses used in COPD has some systemic side effects and increases the risk of developing pneumonia.
Theophylline
Peter J. Barnes
Pharmaceuticals , 2010, DOI: 10.3390/ph3030725
Abstract: Theophylline (3-methyxanthine) has been used to treat airway diseases for over 70 years. It was originally used as a bronchodilator but the relatively high doses required are associated with frequent side effects, so its use declined as inhaled β 2-agonists became more widely used. More recently it has been shown to have anti-inflammatory effects in asthma and COPD at lower concentrations. The molecular mechanism of bronchodilatation is inhibition of phosphodiesterase(PDE)3 and PDE4, but the anti-inflammatory effect may be due to histone deacetylase (HDAC) activation, resulting in switching off of activated inflammatory genes. Through this mechanism theophylline also reverses corticosteroid resistance and this may be of particular value in severe asthma and COPD where HDAC2 activity is markedly reduced. Theophylline is given systemically (orally as slow-release preparations for chronic treatment and intravenously for acute exacerbations of asthma) and blood concentrations are determined mainly by hepatic metabolism, which may be increased or decreased in several diseases and by concomitant drug therapy. Theophylline is now usually used as an add-on therapy in asthma patients not well controlled on inhaled corticosteroids and in COPD patients with severe disease not controlled by bronchodilator therapy. Side effects are related to plasma concentrations and include nausea, vomiting and headaches due to PDE inhibition and at higher concentrations to cardiac arrhythmias and seizures due to adenosine A 1-receptor antagonism.
Th2 cytokines and asthma: an introduction
Peter J Barnes
Respiratory Research , 2001, DOI: 10.1186/rr39
Abstract: In this issue of Respiratory Research we focus on Th2 cytokines and their potential role in allergic diseases, such as asthma. John Steinke and Larry Borish [4] discuss the role of IL-4 in the pathogenesis of asthma and make the point that this is an upstream cytokine that regulates allergic inflammation by promoting Th2 cell differentiation and IgE synthesis. Early studies with an IL-4 antagonist, soluble recombinant IL-4 receptor (altrakincept), show therapeutic benefit as a steroid-replacing agent in moderately severe asthma [5] and longer term clinical trials are now underway. IL-5 is discussed by Scott Greenfeder and colleagues [6]. IL-5 is a cytokine that is highly specific for eosinophilic inflammation and antibodies that block IL-5 actions are effective in reducing eosinophilic inflammation and airway hyperresponsiveness (AHR) in various species. Recently, studies of a humanised anti-IL-5 monoclonal antibody (mepomizulab) in asthmatic patients have confirmed its extraordinary efficacy in reducing eosinophils in the circulation and the airways, but surprisingly no reduction in response to allergen or in AHR [7]. This result has been confirmed in a preliminary clinical trial of asthmatic patients whose symptoms were not controlled with inhaled corticosteroids and who showed no clinical improvement with anti-IL-5 antibody, despite a marked suppression of circulating eosinophils [8]. These studies confirm the importance of IL-5 in eosinophilic inflammation in man, but question the role of eosinophils in asthma. IL-13 has many actions similar to those of IL-4 and also regulates IgE production but, unlike IL-4, it does not regulate T cell differentiation to Th2 cells and T lymphocytes do not respond to IL-13. The role of IL-13 in asthma was recently reviewed in this journal by Marsha Wills-Carp [9]. IL-9 has been less intensively investigated than the other Th2 cytokines, but appears to amplify Th2-cell-mediated responses, as reviewed by Roy Levitt and colleagues
Respiratory Research: a new multidisciplinary journal for a new age (http://respiratory-research.com)
Peter J Barnes
Respiratory Research , 2000, DOI: 10.1186/rr1
Abstract: It is true that respiratory medicine is already well served by several specialist journals, but it is also true that it remains difficult to keep track of the overwhelming amount of new information being published. This is particularly the case in rapidly developing fields such as molecular and cell biology and molecular genetics. Many important advances in the basic sciences are of great relevance to respiratory medicine, but are difficult to assimilate, particularly when the developments take place in areas outside respiratory medicine. Respiratory Research aims to take a multidisciplinary approach and bring together aspects of basic science that are relevant to clinical respiratory medicine. This will be facilitated by a strong team of 17 internationally recognised Associate Editors, who have each nominated members of the Editorial Board in order to give the widest possible perspective. We hope that this active editorial team will play a decisive role in selecting authors for timely reviews and comments on recently published research from within and outside the field of respiratory medicine. The bringing together of approaches drawn from many different disciplines, including molecular genetics, molecular and cell biology, biochemistry, physiology, pharmacology, clinical medicine and epidemiology will allow the journal to cover the many areas of research that have an impact on respiratory medicine.Although the journal is primarily aimed at those involved in academic respiratory research, we hope that it will also be popular with those in clinical respiratory medicine since it will highlight the latest scientific developments relevant to respiratory medicine in an easily digested format. Respiratory medicine is a complicated discipline, as the structure of the lung is highly complex and diverse. This necessitates a wide variety of approaches to understand pulmonary diseases. The relative availability of lung cells for investigation makes this a speciality that is r
Molecular mechanisms of atopy
Peter J. Barnes
Mediators of Inflammation , 2001, DOI: 10.1080/09629350120102000
Abstract:
Characterization of T Lymphocytes in Chronic Obstructive Pulmonary Disease
Peter J Barnes,Manuel G Cosio
PLOS Medicine , 2004, DOI: 10.1371/journal.pmed.0010020
Abstract:
Defects of Protein Phosphatase 2A Causes Corticosteroid Insensitivity in Severe Asthma
Yoshiki Kobayashi, Nicolas Mercado, Peter J. Barnes, Kazuhiro Ito
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027627
Abstract: Background Corticosteroid insensitivity is a major barrier of treatment for some chronic inflammatory diseases, such as severe asthma, but the molecular mechanism of the insensitivity has not been fully elucidated. The object of this study is to investigate the role of protein phosphate 2A (PP2A), a serine/threonine phosphatase, on corticosteroid sensitivity in severe asthma. Methodology/Principal Findings Corticosteroid sensitivity was determined by the dexamethasone ability to inhibit TNFα-induced IL-8 or LPS-induced TNFα production. PP2A expression, glucocorticoid receptor (GR) nuclear translocation defined as the nuclear/cytoplasmic GR ratio and phosphorylation of GR-Ser226, c-Jun N-terminal kinase 1 (JNK1) and PP2A were analysed by Western-blotting. Phosphatase activity was measured by fluorescence-based assay. Okadaic acid (OA), a PP2A inhibitor, reduced corticosteroid sensitivity with reduced GR nuclear translocation and increased GR phosphorylation in U937 monocytic cells. PP2A knockdown by RNA interference showed similar effects. IL-2/IL-4 treatment to U937 reduced corticosteroid sensitivity, and PP2A expression/activity. In peripheral blood mononuclear cells (PBMCs) from severe asthma, the PP2A expression and activity were significantly reduced with concomitant enhancement of PP2AC-Tyr307 phosphorylation compared with those in healthy volunteers. As the results, GR-Ser226 and JNK1 phosphorylation were increased. The expression and activity of PP2A were negatively correlated with phosphorylation levels of GR-Ser226. Furthermore, co-immunoprecipitation assay in U937 cells revealed that PP2A associated with GR and JNK1 and IL-2/IL-4 exposure caused dissociation of each molecule. Lastly, PP2A overexpression increased corticosteroid sensitivity in U937 cells. Conclusions/Significance PP2A regulates GR nuclear translocation and corticosteroid sensitivity possibly by dephosphorylation of GR-Ser226 via dephosphorylation of upstream JNK1. This novel mechanism will provide new insight for the development of new therapy for severe asthma.
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