I am interested in the cells, soluble mediators and receptors that collectively help switch inflammation off, so-called inflammatory resolution. My overall hypothesis is that understanding how acute inflammation resolves will provide insight into the aetiology of chronic inflammatory diseases. In addition, identifying mediators and receptors essential for resolution will help develop drugs that will drive ongoing inflammation down a pro-resolution pathway. However, recent work suggests that resolution of acute inflammation is not the end of immune responses to infection/injury but, that through cells of the mononuclear phagocyte system expressing arachidonic acid, docosahexaenoic acid and eicosapentaenoic acid metabolising enzymes resolution acts as a bridge between innate and adaptive immunity. We believe that defects in these pathways may contribute to the aetiology of, for instance, “inflammaging” and that rectifying these defects may improve vaccine efficacy in the elderly. To understand these processes better as they pertain to humans and human ageing, we have developed models of acute, self-limiting inflammation in healthy volunteers. As a result of these studies we are mapping pathways of inflammation with emphasis on mononuclear phagocytes and lipid mediators and are finding clear differences between young and older individuals with regard to pro-resolution processes. In my presentation, I will present these new data and speculate on their potential contribution to the aetiology of chronic inflammation and the role ageing plays in this process.