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lüll Lipid mediators as agonists for the resolution of acute lung inflammation and injury Bonnans C; Levy BDAm J Respir Cell Mol Biol 2007[Feb]; 36 (2): 201-5Resolution of acute lung inflammation and injury is an active process; it is not merely the absence of proinflammatory signals. Restoration of homeostasis is coordinated by specific mediators and cellular events. In response to injury and inflammatory stimuli, infiltrating leukocytes and tissue-resident cells interact to generate lipoxins (LXs), which are bioactive eicosanoids derived from arachidonic acid. In contrast to proinflammatory leukotrienes and prostaglandins, LXs display potent antiinflammatory actions. LXA(4) interacts with a G protein-coupled receptor, termed ALX, that transduces counter-regulatory signals in part via intracellular polyisoprenyl phosphate remodeling. Presqualene diphosphate (PSDP) is a polyisoprenyl phosphate in human neutrophils that is rapidly converted to presqualene monophosphate (PSMP) upon cell activation. PSDP, but not PSMP, directly inhibits phospholipase D, phosphoinositol-3 kinase, and superoxide anion generation. LXs block PSDP turnover in neutrophil membranes to prevent proinflammatory responses. Hence, LX and polyisoprenyl phosphate signaling provide a counter-regulatory circuit to promote resolution of acute lung inflammation. LXA(4) and PSDP mimetics have been prepared with potent protective actions in murine models of asthma and acute lung injury.|Animals[MESH]|Humans[MESH]|Leukocytes, Mononuclear/drug effects/immunology[MESH]|Lipoxins/*pharmacology[MESH]|Pneumonia/*pathology/*therapy[MESH]|Polyisoprenyl Phosphates/chemistry[MESH]|Receptors, Lipoxin/immunology[MESH]|Respiratory Distress Syndrome/*pathology/*therapy[MESH] |