eicosatetraenoate products; this step catalyzed by 5-lipoxygenase (ALOX5). Accordingly, these double oxygenations yield either 5,6,15-trihydroxy- or 5,14,15-trihydroxy-eicosatetraenoates. The double oxygenations may be conducted within a single cell type which possess ALOX5 and an enzyme with 15-lipoxygenase activity or, alternatively, by two different cell types, each of which possesses one of these enzyme activities. In the latter transcellular biosynthetic pathway, one cell type forms either the 5,6-dihydroxy-, 5-hydroxy, 14,15-dihydroxy- or a 15-hydroxy-eicosatetraenoate, and then passes this intermediate to a second cell type, which metabolizes it to the final LX product. For example, LXs are formed by platelets which, lacking ALOX5, cannot synthesize them. Rather, neutrophils form, the 5,6-epoxide, leukotriene A4 (LTA4), via ALOX5 and passed it to platelets that then reduce it a 5,6-dihydroxy-eicosateteraenoate product and further metabolize it through ALOX12 to form the 15-hydroxy product, LXA4. The two LXs are distinguished form their 15-epi-LTX epimers by their structural formulae: LxA4: 5S,6R,15S-trihydroxy-7E,9E,11Z,13E-eicosatetraenoic acid LxB4: 5S,14R,15S-trihydroxy-6E,8Z,10E,12E-eicosatetraenoic acid 15-epi-LxA4: 5S,6R,15R-trihydroxy-7E,9E,11Z,13E-eicosatetraenoic acid 15-epi-LxB4: 5S,14R,15R-trihydroxy-6E,8Z,10E,12E-eicosatrienoic acid Note that the two LXs have their 15-hydroxyl residues in the S chirality configuration because all of the ALOX enzymes form 15S-hydroxy AA products. In contrast, the 15-hydroxy residues of the two epi-LXs are 15R chirality products because they are synthesized by aspirin-treated cyclooxygenase 2 or the microsomal, mitochondrial, or bacterial Cytochrome P450s; these enzymes form almost entirely or partly 15R-hydroxy products. (15-Epi-LTA44 and 15-epi-LTB44 are sometimes termed AT-LxA4 and AT-LxB4, respectively, when acknowledging their formation by aspirin-treated cyclooxygenase 2, i.e. by Aspirin-Triggered cyclooxygenase 2.) In addition to the pathways cited above, other transcellular metabolic routes have been shown to make LXs. For example, 5-lipoxygenase (i.e. (ALOX5) in neutrophils and 15-lipoxygenase-1 (i.e. ALOX15) in immature erythrocytes and reticulocytes operate in series to form LxA44 and LxB44; this pathway also occurs in serial interactions between neutrophils and eosinophils; between epithelium or M2 Macrophages/monocytes and neutrophils; and endothelium or skeletal muscle and neutrophils. Stimulation of synthesis The lipoxins commonly form as a consequence of stimulating the production of pro-inflammatory arachidonic acid metabolites. However, certain cytokines such as IFN-γ and IL-1β further increase production of the lipoxins (as well as other anti-inflammatory PUFA metabolites and proteins, e.g. IL4. Further metabolism LXs are rapidly metabolized, mainly by macrophages, to inactive products by being oxidized at carbon 15 to form 15-keto (also termed 15-oxo) LX products by a 15-hydroxyprostaglandin dehydrogenase; 15-oxo-LXA4 may be further metabolized to 13,14-dihydro-LXA4 by an oxidoreductase. 15-Epi-LXA4 and 15-epi-LXB4 are