Identification of altered mechanisms in the bronchial epithelium in asthma using transcriptomics and functional assays  

Asthma is a common chronic disease with an estimated 300 million affected individuals. Worldwide, deaths from asthma have reached more than 180,000 annually. There is accumulating evidence that the airway epithelium is intrinsically different in asthma if compared with the normal type. For example, bronchial epithelial cells isolated from asthma patients and cultured in vitro have: (a) defective repair mechanisms, (b) altered barrier properties including reduced tight junction protein expression and formation, (c) elevated expression of pro-remodelling factors, and when differentiated have increased numbers of goblet and reduced numbers of ciliated cells. This led to the hypothesis that the airway epithelium contributes to disease etiology, however detailed understanding of which mechanisms may be altered is lacking at this time and similarly novel approaches to target the epithelium may have utility in asthma. We have recently completed transcriptomic analyses of bronchial epithelial cells isolated from asthma and control subject and identified differential expression of genes/pathways.

This studentship aims to i) translate our initial transcriptomic findings to greater understanding of intrinsic differences and altered biology in asthma patient lung cells and ii) investigate approaches to influence the airway epithelium to improve properties potentially deficient in asthma.

Available to Home/EU/International students

Please email a CV with a covering letter to Professor Ian Sayers.