Innate Immunity in COPD version 1

  • Research type

    Research Study

  • Full title

    Analysis of innate immune competence in people with chronic obstructive pulmonary disease (COPD).

  • IRAS ID

    320686

  • Contact name

    David H. Dockrell

  • Contact email

    David.Dockrell@ed.ac.uk

  • Sponsor organisation

    University of Edinburgh

  • Duration of Study in the UK

    4 years, 8 months, 18 days

  • Research summary

    Chronic Obstructive Pulmonary Disease (COPD) causes obstruction to airflow when breathing out. It is a leading cause of chronic lung disease, hospitalization and death. Smoking is the major cause of COPD but why some smokers develop COPD while others do not is poorly understood. A central feature of COPD is accumulation of inflammatory blood cells, macrophages and neutrophils, in the airway, leading to lung injury and airway damage. The small airways of many patients with COPD contain bacteria, which are absent in healthy smokers or non-smokers. These bacteria stimulate recruitment of neutrophils, macrophages and other inflammatory cells, further accelerating airway injury. We and others have shown resident macrophages in the lung and inflammatory cells (neutrophils and macrophages) recruited from the blood, which normally clear bacteria, have reduced anti-bacterial capacity in COPD and that their altered function impairs the resolution of inflammation. We now wish to test why these cells fail to clear bacteria focusing in particular on how they use molecules as food to generate energy, a process termed metabolism, since we know this is an important determinant of immune cell function. Comparison will be made between lung resident cells (obtained by performing bronchoscopy and washing a segment of lung to flush out immune cells) and those from the blood to determine if the alterations are specific to the lung. We will identify alterations in responses to bacteria in relation to changes in metabolism . A major focus will be on how structures in the cell that normally are key for energy production (i.e. mitochondria) become dysfunctional and how this impacts responses to bacteria. We will relate findings to the clinical features of COPD and to healthy non-smokers and smokers to separate smoking-related changes from COPD. Our aim is to develop new approaches with which to treat and manage COPD.

  • REC name

    West of Scotland REC 5

  • REC reference

    23/WS/0044

  • Date of REC Opinion

    26 Apr 2023

  • REC opinion

    Further Information Favourable Opinion