Functional arrays of lipid signals generated via transcellular processing ω-3 PUFA: endogenous inhibitors of microinflammation. At sites where COX-2 is expressed and treated with NSAIDs, although PG formation is blocked, systemic ω-3 PUFA can be converted via a COX-2-NSAID–dependent LO-type mechanism (stereospecific hydrogen abstraction at C16 or C13 in C20:5 to give R insertions of molecular O₂) to yield 15R-H(p)EPE or 18R-H(p)EPE. These compounds are reduced to alcohols and converted to epoxide intermediates. Elucidation of the complete stereochemistry of the trihydroxy-compounds is in progress, and they are depicted in their likely configuration. The products interact with cells in the local microenvironment, inhibiting PMN recruitment. See text and suggested reading list (http://www.jci.org/cgi/content/full/107/12/1481/DC1) for details.