Lipoxin A₄ yields an electrophilic 15-oxo metabolite that mediates FPR2 receptor-independent anti-inflammatory signaling.

ABSTRACT: The enzymatic oxidation of arachidonic acid is proposed to yield trihydroxytetraene species (termed lipoxins) that resolve inflammation via ligand activation of the formyl peptide receptor, FPR2. While cell and murine models activate signaling responses to synthetic lipoxins, primarily 5S,6R,15S-trihydroxy-7E,9E,11Z,13E-eicosatetraenoic acid (lipoxin A₄, LXA₄), there are expanding concerns about the biological formation, detection and signaling mechanisms ascribed to LXA₄ and related di- and tri-hydroxy ω-6 and ω-3 fatty acids. Herein, the generation and actions of LXA₄ and its primary 15-oxo metabolite were assessed in control, LPS-activated and arachidonic acid supplemented RAW 264.7 macrophages.

SUBMITTER: Koudelka A 

PROVIDER: S-EPMC10871244 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature