In vivo biosynthesis of LXA4 is triggered in an acute inflammatory process in which Polymorphonuclear neutrophil (PMN)’s interaction with PGE2 and PGD2 activates 15-lipoxygenase subsequently facilitating LXA4 biosynthesis (Claria and Serhan 1995). In a murine peritonitis model, the maximum level of LXA4 was achieved within 2 hours and gradually decreased during the first 24 hours (Bannenberg et al. 2005). The formation of LXs is preserved across a wide range of animal species, from fish to humans (Levy 2005). This indicates the physiological importance of LXs.