51
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Recent advances in pre-clinical mouse models of COPD

      review-article
      * , *
      Clinical Science (London, England : 1979)
      Portland Press Ltd.
      acute exacerbations of chronic obstructive pulmonary disease (AECOPD), chronic obstructive pulmonary disease (COPD), emphysema, inflammation, skeletal muscle wasting, smoking, AECOPD, acute exacerbations of COPD, BAL, bronchoalveolar lavage, BALF, BAL fluid, COPD, chronic obstructive pulmonary disease, GM-CSF, granulocyte/macrophage colony-stimulating factor, GOLD, Global initiative on chronic Obstructive Lung Disease, Gpx, glutathione peroxidase, HDAC, histone deacetylation, IL, interleukin, LTB4, leukotriene B4, MAPK, mitogen-activated protein kinase, MCP-1, monocyte chemotactic protein-1, MMP, matrix metalloproteinase, NE, neutrophil elastase, NF-κB, nuclear factor κB, Nrf2, nuclear erythroid-related factor 2, O2•−, superoxide radical, ONOO−, peroxynitrite, PDE, phosphodiesterase, PI3K, phosphoinositide 3-kinase, ROS, reactive oxygen species, RV, rhinovirus, SLPI, secretory leucocyte protease inhibitor, SOD, superoxide dismutase, TGF-β, transforming growth factor-β, TIMP, tissue inhibitor of metalloproteinases, TNF-α, tumour necrosis factor-α, V/Q, ventilation/perfusion

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          COPD (chronic obstructive pulmonary disease) is a major incurable global health burden and will become the third largest cause of death in the world by 2020. It is currently believed that an exaggerated inflammatory response to inhaled irritants, in particular cigarette smoke, causes progressive airflow limitation. This inflammation, where macrophages, neutrophils and T-cells are prominent, leads to oxidative stress, emphysema, small airways fibrosis and mucus hypersecretion. The mechanisms and mediators that drive the induction and progression of chronic inflammation, emphysema and altered lung function are poorly understood. Current treatments have limited efficacy in inhibiting chronic inflammation, do not reverse the pathology of disease and fail to modify the factors that initiate and drive the long-term progression of disease. Therefore there is a clear need for new therapies that can prevent the induction and progression of COPD. Animal modelling systems that accurately reflect disease pathophysiology continue to be essential to the development of new therapies. The present review highlights some of the mouse models used to define the cellular, molecular and pathological consequences of cigarette smoke exposure and whether they can be used to predict the efficacy of new therapeutics for COPD.

          Related collections

          Most cited references137

          • Record: found
          • Abstract: not found
          • Article: not found

          Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Association between chronic obstructive pulmonary disease and systemic inflammation: a systematic review and a meta-analysis.

            Individuals with chronic obstructive pulmonary disease (COPD) are at increased risk of cardiovascular diseases, osteoporosis, and muscle wasting. Systemic inflammation may be involved in the pathogenesis of these disorders. A study was undertaken to determine whether systemic inflammation is present in stable COPD. A systematic review was conducted of studies which reported on the relationship between COPD, forced expiratory volume in 1 second (FEV(1)) or forced vital capacity (FVC), and levels of various systemic inflammatory markers: C-reactive protein (CRP), fibrinogen, leucocytes, tumour necrosis factor-alpha (TNF-alpha), and interleukins 6 and 8. Where possible the results were pooled together to produce a summary estimate using a random or fixed effects model. Fourteen original studies were identified. Overall, the standardised mean difference in the CRP level between COPD and control subjects was 0.53 units (95% confidence interval (CI) 0.34 to 0.72). The standardised mean difference in the fibrinogen level was 0.47 units (95% CI 0.29 to 0.65). Circulating leucocytes were also higher in COPD than in control subjects (standardised mean difference 0.44 units (95% CI 0.20 to 0.67)), as were serum TNF-alpha levels (standardised mean difference 0.59 units (95% CI 0.29 to 0.89)). Reduced lung function is associated with increased levels of systemic inflammatory markers which may have important pathophysiological and therapeutic implications for subjects with stable COPD.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              The global burden of disease, 1990-2020.

                Bookmark

                Author and article information

                Journal
                Clin Sci (Lond)
                Clin. Sci
                cls
                CS
                Clinical Science (London, England : 1979)
                Portland Press Ltd.
                0143-5221
                1470-8736
                14 October 2013
                1 February 2014
                : 126
                : Pt 4
                : 253-265
                Affiliations
                *Lung Health Research Centre, Department of Pharmacology, University of Melbourne, Parkville, VIC 3010, Australia
                Author notes
                Correspondence: Associate Professor Ross Vlahos (email rossv@ 123456unimelb.edu.au ).
                Article
                CS20130182
                10.1042/CS20130182
                3878607
                24144354
                5463c1fa-458d-4899-b647-eebdacb2db14
                © 2014 The author(s) has paid for this article to be freely available under the terms of the Creative Commons Attribution Licence (CC-BY)(http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 4 April 2013
                : 17 July 2013
                : 1 August 2013
                Page count
                Figures: 1, Tables: 1, References: 140, Pages: 13
                Categories
                Review Article
                S8

                Medicine
                smoking,copd, chronic obstructive pulmonary disease,gm-csf, granulocyte/macrophage colony-stimulating factor,gold, global initiative on chronic obstructive lung disease,gpx, glutathione peroxidase,hdac, histone deacetylation,ltb4, leukotriene b4,mcp-1, monocyte chemotactic protein-1,ne, neutrophil elastase,nrf2, nuclear erythroid-related factor 2,onoo−, peroxynitrite,pde, phosphodiesterase,ros, reactive oxygen species,tgf-β, transforming growth factor-β,tnf-α, tumour necrosis factor-α,v/q, ventilation/perfusion,acute exacerbations of chronic obstructive pulmonary disease (aecopd),chronic obstructive pulmonary disease (copd),emphysema,inflammation,skeletal muscle wasting,aecopd, acute exacerbations of copd,bal, bronchoalveolar lavage,balf, bal fluid,il, interleukin,mapk, mitogen-activated protein kinase,mmp, matrix metalloproteinase,nf-κb, nuclear factor κb,o2•−, superoxide radical,pi3k, phosphoinositide 3-kinase,rv, rhinovirus,slpi, secretory leucocyte protease inhibitor,sod, superoxide dismutase,timp, tissue inhibitor of metalloproteinases

                Comments

                Comment on this article