Understanding common drivers of dysfunction in chronic respiratory diseases

Chronic respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis (PF), represent significant health burdens worldwide yet their pathogenic mechanisms remain poorly understood.

COPD is characterised by persistent airflow obstruction, chronic inflammation and tissue remodelling, whilst PF is characterised by chronic, progressive scarring of the lungs through dysfunctional regenerative/repair processes, excess collagen deposition, and exaggerated growth factor release. This results in tissue stiffening and impaired gas exchange.

Despite their differing pathologies, both conditions are characterised by development of small airways disease (SAD) – thickening/fibrosis of small bronchioles and emphysema – destruction of alveolar walls, leading to airspace enlargement and compromised lung function.

Despite their paradoxical nature both pathologies coexist in COPD and PF patients, highlighting the need to understand their common underlying mechanisms.

Dysfunctional repair processes are key to both conditions suggesting shared pathogenic mechanisms. Drivers such as urban particulate matter, oxidative stress and infection are implicated as potential drivers of these processes.

Research Aims

This project aims to elucidate the common drivers of dysfunction that contribute to the paradoxical processes of tissue destruction in airway remodelling and excessive/dysregulated repair in fibrosis. The specific objectives are:

The specific objectives are:

1. Establish an ex vivo model to characterize cellular interactions between innate immune cells, epithelial cells, and fibroblasts using COPD/PF patient samples.

2. Identify shared pathogenic mechanisms: Using this ex vivo model, investigate potential drivers of dysfunction to examine factors which influence these dysregulated repair pathways.

3. Evaluate biomarkers and therapeutic targets: Identify potential biomarkers for early detection and novel therapeutic targets at early intervention points in the shared pathogenic pathway.

The study will provide a better understanding of the complex the interplay between tissue destruction/ airway remodelling, and excessive repair in chronic respiratory diseases. This research has the potential to bridge the gap between the distinct but interconnected processes of emphysema and SAD.

In defining the drivers and shared pathways of effect, we can develop novel therapeutic strategies that could potentially mitigate the dysregulated repair processes common to these diseases and offer novel therapeutic options to millions of chronic respiratory disease patients. 

Person Specification

Applicants should have a strong background in Biomedical science, and ideally a background in molecular biology. They should have a commitment to research in Respiratory science and hold or realistically expect to obtain at least an Upper Second-Class Honours Degree in a relevant subject.

How to apply

Informal enquiries should be directed to Aaron Scott

Applications should be directed to Aaron Scott (email a.scott@bham.ac.uk). To apply, please send:

•          A detailed CV, including your nationality and country of birth;

•          Names and addresses of two referees;

•          A covering letter highlighting your research experience/capabilities;

•          Copies of your degree certificates with transcripts;

•          Evidence of your proficiency in the English language, if applicable.