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Ethanol treatment led to marked lipid dysregulation in alveolar macrophages, which significantly impaired the glycolytic response to LPS, thus weakening the cells’ ability to mount effective immune responses.87 Ethanol exposure also inhibited AMP-activated protein kinase signaling and phagocytosis in alveolar macrophages, with ethanol metabolism playing a central role in these impairments.88 Additionally, ethanol exposure led to marked increases in mitochondrial DNA (mtDNA) damage.96 Specifically, exosomes isolated from ethanol-exposed mouse alveolar macrophages increased mtDNA damage and barrier dysfunction in a mouse alveolar epithelial cell line