Purpose: Methods: An ARDS rat model was established by intratracheal instillation of lipopolysaccharide (LPS). Rats were randomly allocated to the control, ARDS, AKK, and EVs groups. Following model establishment, AKK or AKK-EVs were administered orally once daily for 7 consecutive days. Lung injury was evaluated by body weight, hematoxylin and eosin staining, lung wet/dry weight ratio, and bronchoalveolar lavage fluid (BALF) analysis. Fecal 16S rRNA sequencing, untargeted metabolomics, lung transcriptomics, and integrated multi-omics analyses were performed. The pulmonary expression of Il17a, Cxcl1, Tnf, and Il6 was validated by qRT-PCR. Results: Compared with the ARDS group, AKK and AKK-EVs attenuated weight loss and lung histopathological injury and reduced the lung wet/dry weight ratio, BALF total cell count and protein concentration, and BALF IL-17A and TNF-α levels. Both interventions partially remodeled the gut microbial community, including changes in Lachnospiraceae_NK4A136_group, norank_f_Muribaculaceae, Bacteroides, and Escherichia-Shigella. Metabolomic changes mainly involved lipid, amino acid, and bile acid metabolism. Lung transcriptomic analysis identified differential enrichment of the IL-17, TNF, chemokine, and cytokine-cytokine receptor interaction pathways. qRT-PCR further showed increased Il17a, Cxcl1, Tnf, and Il6 expression in the ARDS group and reduced expression following AKK or AKK-EVs intervention. Integrated analyses identified associations among alterations in gut microbiota, metabolites, and pulmonary gene expression. Conclusion: AKK and AKK-EVs alleviated LPS-induced ARDS, accompanied by remodeling of gut microbial and metabolic profiles and attenuation of pulmonary IL-17- and TNF-related inflammatory signaling. AKK-EVs may represent a potential cell-free intervention for ARDS.