Airway remodelling in asthma is categorised by airway smooth muscle hypertrophy and hyperplasia, change in the type and amount of the extra cellular matrix and epithelial shedding and mucous gland hyperplasia. Our interest is how airway proteases and myofibroblast / extra cellular matrix interactions effect myofibroblast growth and behaviour. These studies employ primary airway cell culture, co-cultures, protein expression, functional activity assay real time PCR and proteomics.

Lymphangioleiomyomatosis (LAM) is a rare lung and lymphatic disease categorised by infiltration of smooth muscle type cells in the lungs and lymphatics leading to progressive respiratory impairment. The disease only effects women and is caused by a defect in one of the two proteins associated with tuberous sclerosis, tuberin and hamartin. Our group has a clinical interest in LAM, runs the UK LAM database and is involved in a number of clinical studies and trials.

Laboratory research projects on LAM include the mechanisms of lung destruction in LAM, prognostic biomarkers and the generation of model systems to study LAM.

Matrix metalloproteinases are proteolytic enzymes secreted by a range of cells and regulated by pro-inflammatory cytokines, growth factors, and extra cellular matrix. We have been studying these in airway myofibroblasts and also specific diseases including chronic obstructive pulmonary disease and LAM.