Eickmeier, O.Seki, H.Haworth, O.Hilberath, JN.Gao, F.Uddin, M.Croze, RH.Carlo, T.Pfeffer, MA.Levy, BD.2014-03-102012Eickmeier, O., H. Seki, O. Haworth, JN. Hilberath, F. Gao, M. Uddin, RH. Croze, T. Carlo, MA. Pfeffer, and BD. Levy. 2012. “Aspirin-Trigge red-Resolvin D1 reduces mucosal inflammation and promotes resolution in a murine model of acute lung injury.” Mucosal immunology 6 (2): 256-266. doi:10.1038/mi.2012.66. http://dx.doi.org/10.1038/mi.2012.66.1933-0219http://nrs.harvard.edu/urn-3:HUL.InstRepos:11877110Acute Lung Injury (ALI) is a severe illness with excess mortality and no specific therapy. Protective actions were recently uncovered for docosahexaenoic acid -derived mediators, including D-series resolvins. Here, we used a murine self-limited model of hydrochloric acid-induced ALI to determine the effects of aspirin-triggered resolvin D1 (AT-RvD1) on mucosal injury. RvD1 and its receptor ALX/FPR2 were identified in murine lung after ALI. AT-RvD1 (~0.5 – 5 μg/kg) decreased peak inflammation, including bronchoalveolar lavage fluid (BALF) neutrophils by ~75%. Animals treated with AT-RvD1 had improved epithelial and endothelial barrier integrity and decreased airway resistance concomitant with increased BALF epinephrine levels. AT-RvD1 inhibited neutrophil-platelet heterotypic interactions by down-regulating both P-selectin and its ligand CD24. AT-RvD1 also significantly decreased levels of BALF pro-inflammatory cytokines, including IL-1β, IL-6, KC and TNF-α, and decreased NF-κB phosphorylated p65 nuclear translocation. Together, these findings indicate that AT-RvD1 displays potent mucosal protection and promotes catabasis after ALI.en-USJournal Article2014-03-1010.1038/mi.2012.66