Mouse-Lung RNA Seq data
Chronic obstructive pulmonary disease (COPD) is a leading cause of smoking-related mortality, with current treatments targeting symptom relief through bronchodilation rather than addressing underlying disease mechanisms. In this study, we investigated the therapeutic effects and molecular mechanisms of Lactococcus lactis MG534 on smoking-induced emphysema. Oral administration of L. lactis MG534 in smoking-exposed mice significantly attenuated alveolar enlargement and reduced inflammatory markers including IFN-? in bronchoalveolar lavage fluid and lung tissue. Transcriptomic analysis revealed that L. lactis MG534 treatment reversed smoking-induced gene expression changes, shifting from inflammatory responses toward cellular repair and regeneration pathways. Key immune marker genes such as Cd8a, Cd8b1, CD69, Gzma, and Gzmb were downregulated with L. lactis MG534 treatment. The probiotic restored microbial balance in both lung and gut microbiomes, reducing pathogenic bacteria in the lungs while increasing beneficial bacteria populations in the gut. Metabolomic analysis demonstrated that L. lactis MG534 treatment mitigated smoking-induced metabolic alterations, particularly increasing levels of Hyodeoxycholic acid, which possesses anti-inflammatory properties, and Methionine sulfoxide, which regulates antioxidant mechanisms. These findings suggest that L. lactis MG534 represents a promising candidate for COPD treatment through multiple mechanisms including immunomodulation, tissue repair promotion, microbial balance restoration, and metabolic profile improvement via the gut-lung axis.