Lipids in Chronic Obstructive Pulmonary Disease: A Target for Future Therapy?
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ABSTRACT:
SUBMITTER: Vlahos R
PROVIDER: S-EPMC7055703 | biostudies-literature |
REPOSITORIES: biostudies-literature
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2014-08-14 | GSE60399 | GEO
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Project description:Chronic obstructive pulmonary disease (COPD) is a common and preventable airway disease causing significant worldwide mortality and morbidity. Lifetime exposure to tobacco smoking and environmental particles are the two major risk factors. Over recent decades, COPD has become a growing public health problem with an increase in incidence. COPD is defined by airflow limitation due to airway inflammation and small airway remodelling coupled to parenchymal lung destruction. Most patients exhibit neutrophil-predominant airway inflammation combined with an increase in macrophages and CD8+ T-cells. Asthma is a heterogeneous chronic inflammatory airway disease. The most studied subtype is type 2 (T2) high eosinophilic asthma, for which there are an increasing number of biologic agents developed. However, both asthma and COPD are complex and share common pathophysiological mechanisms. They are known as overlapping syndromes as approximately 40% of patients with COPD present an eosinophilic airway inflammation. Several studies suggest a putative role of eosinophilia in lung function decline and COPD exacerbation. Recently, pharmacological agents targeting eosinophilic traits in uncontrolled eosinophilic asthma, especially monoclonal antibodies directed against interleukins (IL-5, IL-4, IL-13) or their receptors, have shown promising results. This review examines data on the rationale for such biological agents and assesses efficacy in T2-endotype COPD patients.
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Project description:AbstractChronic obstructive pulmonary disease (COPD), characterized by persistent and not fully reversible airflow restrictions, is currently one of the most widespread chronic lung diseases in the world. The most common symptoms of COPD are cough, expectoration, and exertional dyspnea. Although various strategies have been developed during the last few decades, current medical treatment for COPD only focuses on the relief of symptoms, and the reversal of lung function deterioration and improvement in patient's quality of life are very limited. Consequently, development of novel effective therapeutic strategies for COPD is urgently needed. Stem cells were known to differentiate into a variety of cell types and used to regenerate lung parenchyma and airway structures. Stem cell therapy is a promising therapeutic strategy that has the potential to restore the lung function and improve the quality of life in patients with COPD. This review summarizes the current state of knowledge regarding the clinical research on the treatment of COPD with mesenchymal stem cells (MSCs) and aims to update the understanding of the role of MSCs in COPD treatment, which may be helpful for developing effective therapeutic strategies in clinical settings.
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Project description:Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow obstruction that is only partly reversible, inflammation in the airways, and systemic effects or comorbities. The main cause is smoking tobacco, but other factors have been identified. Several pathobiological processes interact on a complex background of genetic determinants, lung growth, and environmental stimuli. The disease is further aggravated by exacerbations, particularly in patients with severe disease, up to 78% of which are due to bacterial infections, viral infections, or both. Comorbidities include ischaemic heart disease, diabetes, and lung cancer. Bronchodilators constitute the mainstay of treatment: β(2) agonists and long-acting anticholinergic agents are frequently used (the former often with inhaled corticosteroids). Besides improving symptoms, these treatments are also thought to lead to some degree of disease modification. Future research should be directed towards the development of agents that notably affect the course of disease.
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Project description:Adult lung resident stem/progenitor cells, including P63+ progenitor cells, have demonstrated the capacity for regeneration of lung epithelium in precinical models. Here we report a clinical trial of intra-pulmonary P63+ progenitor cell transplantation which included 28 participants with chronic obstructive pulmonary disease (COPD) (stage II~IV). For control group, standard of care (SOC) for COPD treatment was given. For intervention group, in addition to SOC, autologous P63+ progenitor cells were isolated from the airway basal layer via bronchoscopic brushing, cultured for 3~5 weeks, and then transplanted into the lungs via bronchoscopy with 0.7-5.2x10^6 cells per kilogram bodyweight. Eventually 20 patients were evaluated (intervention group n=17; control group n=3). No grade 3~5 adverse events (AE) or serious adverse events occurred in any group. Bronchoscopy-associated AEs were recorded only in intervention groups, while the other AEs were recorded in both groups without showing significant difference. Participants in intervention group displayed significant improvement in diffusing capacity of the lung for carbon monoxide (DLCO) (change from baseline, 24 weeks: +18.2%), showing significant difference comparing to control group (change from baseline, 24 weeks: -17.4%)(p-value=0.008). Furthermore, more participants in intervention group showed > 30 m increase in walking distance within 6 minutes, demonstrating significant difference comparing to control group (p-value=0.036). Transcriptomic analysis of cells isolated from responding and non-responding individuals in the intervention group showed that higher expression of P63 and Nkx homeobox-1 was associated with better efficacy. In conclusion, transplantation of cultured P63+ lung progenitor cells was safe and represented a potential treatment strategy for COPD.
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