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      Understanding the role of neutrophils in chronic inflammatory airway disease

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          Abstract

          Airway neutrophilia is a common feature of many chronic inflammatory lung diseases and is associated with disease progression, often regardless of the initiating cause. Neutrophils and their products are thought to be key mediators of the inflammatory changes in the airways of patients with chronic obstructive pulmonary disease (COPD) and have been shown to cause many of the pathological features associated with disease, including emphysema and mucus hypersecretion. Patients with COPD also have high rates of bacterial colonisation and recurrent infective exacerbations, suggesting that neutrophil host defence mechanisms are impaired, a concept supported by studies showing alterations to neutrophil migration, degranulation and reactive oxygen species production in cells isolated from patients with COPD. Although the role of neutrophils is best described in COPD, many of the pathological features of this disease are not unique to COPD and also feature in other chronic inflammatory airway diseases, including asthma, cystic fibrosis, alpha-1 anti-trypsin deficiency, and bronchiectasis. There is increasing evidence for immune cell dysfunction contributing to inflammation in many of these diseases, focusing interest on the neutrophil as a key driver of pulmonary inflammation and a potential therapeutic target than spans diseases. This review discusses the evidence for neutrophilic involvement in COPD and also considers their roles in alpha-1 anti-trypsin deficiency, bronchiectasis, asthma, and cystic fibrosis. We provide an in-depth assessment of the role of the neutrophil in each of these conditions, exploring recent advances in understanding, and finally discussing the possibility of common mechanisms across diseases.

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          Most cited references 137

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          Airway mucus function and dysfunction.

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            Chronic obstructive pulmonary disease

            Summary 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: β2 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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              Granules of the human neutrophilic polymorphonuclear leukocyte.

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                Author and article information

                Contributors
                Role: Writing – Original Draft Preparation
                Role: Writing – Original Draft Preparation
                Role: ConceptualizationRole: Funding AcquisitionRole: SupervisionRole: Writing – Review & Editing
                Role: ConceptualizationRole: SupervisionRole: Writing – Original Draft PreparationRole: Writing – Review & Editing
                Journal
                F1000Res
                F1000Res
                F1000Research
                F1000Research
                F1000 Research Limited (London, UK )
                2046-1402
                26 April 2019
                2019
                : 8
                Affiliations
                [1 ]Birmingham Acute Care Research, Institute of Inflammation and Ageing, University of Birmingham, UK, Birmingham, B15 2TT, UK
                Author notes

                No competing interests were disclosed.

                Article
                10.12688/f1000research.18411.1
                6489989
                Copyright: © 2019 Jasper AE et al.

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

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                Funding
                Funded by: Medical Research Council
                Funded by: Alpha-1 Foundation
                Funded by: National Institute for Health Research
                Funded by: Wellcome Trust
                This work was supported by the Alpha-1 Foundation, the Medical Research Council, the Wellcome Trust, and the National Institute for Health Research.
                The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
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