Endogenous chemical mediators or autacoids play key roles in controlling inflammation and
its programmed resolution. Among them, it is known that lipoxins (LX) and aspirin-triggered
LX (ATL) evoke bioactions in a range of physiologic and pathophysiologic processes and
serve as endogenous lipid/chemical mediators that stop neutrophilic infiltration and initiate
resolution. LXA4, ATL and their metabolic stable analogs elicit cellular responses and
regulate PMN in vivo via interacting with their specific receptor, namely ALX. ALX is the first …