Inflammation is normally a protective response which is vital to the continuing well being of complex organisms. It is initiated in response to an invasion of the host by pathogens, mechanical trauma, toxins or neoplasm and attempts to destroy, dilute or wall-off the inflammatory stimuli or damaged host tissue. The inflammatory response itself involves the interaction of vasculature and cellular processes which are themselves controlled by a myriad of biological mediators. An insufficient inflammatory response renders the individual susceptible to opportunistic infection while an excessive/inappropriate inflammatory response leads to chronic inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. The main aim of our research is to understand the mechanisms which underlie the transition from resolving "physiological" inflammation to chronic "pathological" inflammation. In particular we are focusing on the dynamics of inflammation and the identification of points of fragility in this response, which when perturbed, could lead to a persistent/excessive inflammation. Specific research projects in our laboratory are, 1) Chronic Granulomatose Disease (CGD) has model to discovering the dynamics and controls points in resolving and non-resolving inflammatory responses. (This in vivo platform is also being developed for drug discovery, allowing the effect of potential drug candidates on physiological and pathophysiological inflammation to be compared). 2) The Heme oxygenase system as a Hub for the convergence of oxidative stress, infection/inflammation and metabolism. 3) Macrophage heterogeneity has a design principal for an efficient inflammatory response. 4) The design of an in vitro dynamic model of human inflammation. (This is a unique model designed to study the dynamics of human inflammation and aid drug discovery). 5) In silco modeling/simulation of inflammation. The underlying philosophy behind our research is that the quantitative modeling of physiological and pathophysiological inflammation can be leveraged against the innate complexity of the response when attempting to identify critical inflammatory pathways and drug targets. It is hoped that this research will help establish a toolbox of methodologies in which the relative contribution of differing pathways/mediators to an inflammatory response and the therapeutic potential of different anti-inflammatory targets can be quantified and prioritized. In addition I am interested in the Translation of academic research into commercial opportunities (technology evaluation, patent application and Business plan development) and in this respect I act as an Business fellow for the London technology Network.