In both cigarette smoke extract (CSE)-induced human bronchial epithelial cells and murine COPD models, BSP treatment activated the NR1H4/FXR pathway via gut microbiota-mediated enrichment of Bacteroides intestinalis, significantly reduced pulmonary cytokine levels (IL-6, TNF-α, and IL-1β; p < 0.01 vs. COPD control), and improved lung function parameters. The gene discussed is IL1B; the disease is chronic obstructive pulmonary disease.