arachidonic acid-derived pro-inflammatory metabolites such as: leukotrienes (LTs), e.g. LTB4, LTB4, LTC4, LTD4, and LTE4; hydroxyeicosatetraenoic acids (HETEs), e.g. 5-HETE and 12-HETE; and oxoeicosanoids (oxo-ETE), e.g. 5-oxo-eicosatetraenoic acid (5-oxo-ETE) and 12-oxo-ETE. These metabolites proceed to act directly or indirectly to recruit circulating leukocytes, tissue macrophages, and tissue dendritic cells to the disturbed tissue site. The consequential congregation of the various cell types promotes transcellular pathways in forming specialized pro-resolving mediators (SPMs), including the LXs, which then proceed to stimulate cellular and tissue responses that trend to reverse the actions of the pro-inflammatory mediators, dampen and reverse the inflammatory response, and initiate tissue repair. LXA4 and 15-epi-LXA4 are high affinity receptor ligands for and activators of the FPR2 receptor. FPR2, which is now termed the ALX, ALX/FPR, or ALX/FPR2 receptor, is a G protein coupled receptor initially identified as a receptor for the leukocyte chemotactic factor, N-Formylmethionine-leucyl-phenylalanine (FMLP), based on its amino acid sequence similarity to the known FMLP receptor, FPR1. At least six homologues of this receptor are found in mice. ALX/FPR is a promiscuous (i.e. interacting with diverse ligands) receptor that binds and is activated by other ligands including: a) various N-formyl oligopeptides that, like FMLP, are either released by microbes and mitochondria or are analogs of those released by microbes and mitochondria; b) microbe-derived non-formyl oligopeptides; c) certain polypeptides that are associated with the development of chronic amyloidosis and/or inflammation including Serum amyloid A (SAA) proteins), a 42-amino acid peptide form Amyloid beta termed Aβ42, Humanin, and a cleaved soluble fragment (amino acids 274-388) from the Urokinase receptor; and d) other SPMs including Resolvins RvD1, RvD2, RvD5, AT-RvD1, and RvD3 (see specialized pro-resolving mediators). LXA4 and 15-epi-LXA4 inhibit chemotaxis, transmigration, superoxide generation, NF-κB activation, and/or generation of pro-inflammatory cytokines (e.g. IL8, IL13, IL12, and IL5) by neutrophils, eosinophils, monocytes, Innate lymphoid cells, and/or macrophages, as well as suppress proliferation and production of IgM and IgG antibodies by B lymphocytes. These actions appear to involve stimulating anti-inflammatory signaling pathways, but also blocking the actions of other ALX/FPR ligands which simulate pro-inflammatory pathways. Transgenic mice made to overexpress ALX/FPR exhibit markedly reduced inflammatory responses to diverse insults. LXA4 and 15-epi-LXA4, when introduced by Intrathecal administration into rodents, suppress the perception of inflammatory pain; this action may involve the ALX/FPR receptor shown to be present on the spinal astrocytes of test animal and, based on studies using 15-epi-LXA, inhibition of the