Dr David Dorward studied medicine at the University of Edinburgh (graduated 2006), during which time he completed an intercalated honours degree in Experimental Pathology.  He went on to complete both Foundation and Core Medical Training in South East Scotland.  His PhD entitled “Evaluating the effects of neutrophil induced 'damage'-associated molecular patterns (DAMPs) in infective lung injury” aims to explore the role of mitochondrial DAMPs in the propagation of pneumonia and to assess potential therapeutic interventions. Despite the widespread use of antibiotics, pneumonia still causes millions of deaths worldwide each year. In response to infection neutrophils, cells vital to the body’s defence mechanism, enter the lung releasing large numbers of bug-killing proteins.  In doing so lung cells are also killed, spilling their contents into the surrounding tissue.  A variety of these products (DAMPs) appear to be crucial in propagating a vicious cycle of neutrophil recruitment and lung damage.  Exactly which DAMPs cause this to occur, and whether different DAMPs are released in different types of pneumonia, is not known.  Dr Dorward's study aims to identify those DAMPs important in severe pneumonia, examine their effects on neutrophil function and assess the effect of blocking the action of specific DAMPs.  Using newly designed imaging techniques it is possible to study individual cells in the laboratory and molecular events within mice with pneumonia in real time.  This helps understand the damaging effects of DAMPs more effectively and identify key areas to target in the development of new drugs to treat pneumonia.

 My main interest is in pulmonary pathology, the role of tissue-derived damage associated molecular patterns and their interaction with cognate receptors on cells of the innate immune system.  In particular, the role of DAMPs in influencing the tumour microenvironment.  Current work is focussed on the G protein coupled receptor formyl peptide receptor 1 which is central in driving neutrophil migration to sites of inflammation while a role in influencing epithelial and tumour cell function is also emerging