This review establishes intestinal microecology as a central regulator of ARDS pathogenesis through bidirectional gut-lung axis interactions, wherein ARDS-induced gut barrier dysfunction (involving TJ disruption, mucin depletion, and antimicrobial peptide suppression) drives dysbiosis and bacterial translocation, while gut-derived metabolites (notably SCFAs) and dysbiotic microbiota exacerbate lung injury via oxidative stress, apoptosis, autophagy, and pyroptosis. Here, MUC5AC is linked to acute respiratory distress syndrome.