Binge ethanol exposure alters alveolar macrophage activation in burn-injured mice (INC5P.329)

Abstract

Abstract Alcohol intoxication is involved in 50% of all burn injuries, resulting in an increased risk of lung infection and failure, relative to burn alone. Our work has shown that in a mouse model of episodic binge ethanol exposure followed by burn injury there is prolonged pulmonary inflammation, relative to burn alone. The magnitude of pulmonary inflammation is mediated in part by alveolar macrophages (AMs), thus we examined the effect of ethanol on AM activation. Thirty minutes after binge ethanol exposure, mice were anesthetized and given a 15% total body surface area dorsal scald injury. At 24 and 72 hrs post-injury bronchoalveolar lavage AM granularity was assessed by flow cytometry using side scatter (SSC). At 24 hrs, 12% of AMs from burn alone had high SSC relative to 1.5% of AMs from sham groups (p<0.05). Only 6% of AMs from combined injured had high SSC. By 72 hrs, 3% of AMs from both burn groups had high SSC. Anti-inflammatory M2 phenotype of high SSC AMs was assessed using M2 marker CD206. At 24 hrs, there was no change in CD206. At 72 hrs, AMs from burn alone had a 43% increase in CD206 relative to sham groups. Giving ethanol prior to burn further elevated the expression of this marker by 46% over burn alone. These data indicate ethanol exposure prior to burn injury can differentially alter AM phenotype at early and later time points.