Lipoxin A4 Attenuates

Background: Acute respiratory distress syndrome (ARDS) remains a severe inflammatory lung disorder with limited disease-modifying therapies. Lipoxin A4 (LXA4) is an endogenous specialized pro-resolving mediator that can modulate macrophage responses; however, its role in bacterial ARDS-like injury and the underlying ALX/FPR2-associated mechanism remain incompletely defined. To determine whether post-injury LXA4 attenuates Methods: Male C57BL/6J mice were randomized to PBS, ARDS, LXA4, or LXA4 + WRW4 groups (n=6 per group per time point). Mice were challenged intratracheally with Results: LXA4 reduced macroscopic and histological lung injury, the lung wet weight-to-body weight ratio, BALF IL-6, IL-1β and TNF-α levels, BALF protein leakage, and BALF bacterial burden after Conclusion: LXA4 alleviates bacterial ARDS-like lung injury in mice and promotes pro-resolving macrophage features, with effects attenuated by ALX/FPR2 antagonism. These findings support LXA4/ALX-FPR2 signaling as a preclinical pro-resolving strategy that warrants validation in cell-specific and clinically representative ARDS models.