It was with tremendous enthusiasm that we endeavoured to compile and edit this volume for Progress in Inflammation Research describing novel findings and developments pertaining to the processes governing the resolution of inflammation. It is perhaps surprising that this topic had, to our knowledge, not previously been covered as a separate subject area in a dedicated monograph given what now seems such an obvious thing to do. Historically, researchers have focussed and have made great advances on the initiation and propagation of inflammation. Little attention had been specifically devoted to elucidating the mechanisms orchestrating the resolution of inflammation, although a variety of mechanisms that limit the inflammatory response had been described (e.g., mediator dissipation and deactivation; exogenous mediator removal or reduction; receptor, cell and tissue desensitisation to mediators; identification of agents with anti-inflammatory potential such as IL-10, IL-1 receptor antagonists, TGF-, etc).
It is now believed that manipulation of more recently described processes, recognised as being actively involved in resolution, are therapeutically manipulatable for the treatment of inflammatory diseases. Indeed, patients with chronic inflammatory diseases are by necessity treated in order to reduce established and persistent inflammation with the added hope of preventing further progression of the inflammatory response. It has recently become evident that many of the anti-inflammatory agents currently used in the clinical setting influence inflammatory resolution. For example, glucocorticoids have been shown to influence processes now recognised as being important mechanisms allowing resolution to occur; namely glucocorticoids trigger apoptosis (programmed cell death) in most leukocytes (the neutrophil however is a notable exception) and augment apoptotic cell clearance by phagocytes. Similarly, aspirin, the most widely used NSAID, is involved in an unorthodox biosynthetic pathway yielding important lipid mediators (e.g., 15-epi-lipoxin A4 and 15-epi-lipoxin B4) actively involved in the resolution process.
