Lipoxin A₄ ELISA Kit

Lipoxin A₄ (LXA₄; Item No. 90410) is a part of the specialized pro-resolving mediator (SPM) family of polyunsaturated fatty acid (PUFA) metabolites.¹ It is formed from arachidonic acid through double lipoxygenase-catalyzed reactions initiated by either 5-lipoxygenase (5-LO) followed by 12-LO/15-LO, with a leukotriene A₄ (LTA₄) intermediate, or by 15-LO followed by 5-LO, with 15(S)-HETE and 5(S)-Hp-15(S)-HETE intermediates. The generation of LXA₄ typically requires transcellular metabolism of arachidonic acid.^1,2 For example, LTA₄ that is synthesized in neutrophils by 5-LO is metabolized to LXA₄ in platelets by 12-LO.²

LXA₄ is released during the resolution phase of inflammation and binds to the G protein-coupled LXA₄ receptor (ALX)/formyl peptide receptor (FPR2), which is located on leukocytes, and induces cell type-specific signaling.1 In macrophages, it activates phosphatidylinositol 3-kinase (PI3K) and AKT, stimulates non-phlogistic phagocytosis of apoptotic leukocytes, and inhibits apoptosis to prolong the phagocytotic phase.^3,4 In neutrophils, it inhibits chemotaxis and transmigration and inhibits production of LTB₄ (Item No. 20110).⁵

Cayman’s LXA₄ ELISA Kit is a competitive assay which can be used for quantification of LXA₄. This assay has been tested in urine, serum, and plasma. The ELISA typically displays an IC₅₀ (50% B/B₀) of approximately 200 pg/ml and a detection limit (80% B/B₀) of approximately 50 pg/ml.

Needed but not supplied: Please download the kit booklet to verify if UltraPure Water (Milli-Q or equivalent) or any other components are needed for this assay.

WARNING This product is not for human or veterinary use.

1. Serhan, C.N., Chiang, N., and Van Dyke, T.E. Resolving inflammation: Dual anti-inflammatory and pro-resolution lipid mediators. Nat. Rev. Immunol. 8(5), 349-361 (2008).

2. Serhan, C.N., and Sheppard, K.-A. Lipoxin formation during human neutrophil-platelet interactions. Evidence for the transformation of leukotriene A₄ by platelet 12-lipoxygenase in vitro. J. Clin. Invest. 85(3), 772-780 (1990).

3. Fierro, I.M., Colgan, S.P., Bernasconi, G., et al. Lipoxin A₄ and aspirin-triggered 15-epi-lipoxin A₄ inhibit human neutrophil migration: Comparisons between synthetic 15 epimers in chemotaxis and transmigration with microvessel endothelial cells and epithelial cells. J. Immunol. 170(5), 2688-2694 (2003).

4. Mitchell, S., Thomas, G., Harvey, K., et al. Lipoxins, aspirin-triggered epi-lipoxins, lipoxin stable analogues, and the resolution of inflammation: Stimulation of macrophage phagocytosis of apoptotic neutrophils in vivo. J. Am. Soc. Nephrol. 13(10), 2497-2507 (2002).

5. Godson, C., Mitchell, S., Harvey, K., et al. Cutting edge: Lipoxins rapidly stimulate nonphlogistic phagocytosis of apoptotic neutrophils by monocyte-derived macrophages. J. Immunol. 164(4), 1663-1667 (2000).

Li, J., Xiao, Y., Zhang, Y., et al. Pulmonary delivery of specialized pro-resolving mediators-based nanotherapeutics attenuates pulmonary fibrosis in preclinical animal models. ACS Nano 17(16), 15354-15370 (2023).