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The process of acute inflammation relies on the active engagement of a series of pro-resolving mediators which assure temporal and spatial containment of the host reaction: a pro-inflammatory phase is followed by an anti-inflammatory and pro-resolving phase in line with “the beginning programmes the end” concept. Within the network of pro-resolving mediators is emerging a pattern of biological properties, shared by a variety of players, rendering specific actions paradigmatic (e.g. promotion of efferocytosis). Harnessing endogenous homeostatic pathways can lead to innovative anti-inflammatory therapeutics with beneficial applications for chronic inflammatory pathologies.
Within this area of investigation, Lipoxin A4 and Annexin A1 are two players able to halt leukocyte migration and promote macrophage phagocytosis of infective agents as well as apoptotic leukocytes. These effects are mediated by a specific receptor, the formyl peptide receptor type 2 (the acronym FPR2/ALX is currently used to identify the human receptor). Generation of a colony of mice deficient in the mouse orthologues of FPR2/ALX is helping elucidate the patho-physiological impact of this receptor (and its agonists) in acute inflammation providing, at the same time, proof-of-concept data for its exploitation in drug discovery programmes.
Supported by the Wellcome Trust (programme programme 086867/Z/08)
