Multi-Omics Reveals Gut-Lung Axis Dysbiosis and Metabolic Shifts in Pulmonary Fibrosis

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Background: The study aims to define time-dependent gut microbiota-metabolite interactions in pulmonary fibrosis (PF) using multi-omics. Methods: C57BL/6 mice (n=60) were divided into bleomycin-induced pulmonary fibrosis and saline control groups, with gut microbiomics, fecal metabolomics, and lung/colon histopathology assessed on days 0, 14, and 28. Results: Temporal analysis showed gut microbiota diversity peaking at 430 OTUs on day 14 and dropping to 252 by day 28. Key taxa included Akkermansia, Allobaculum, Limosilactobacillus, and Ligilactobacillus. Key metabolites were campesterol, cholesterol, 9-oxoandrost-4-ene-3,17-dione, 3β-hydroxypregn-5-en-20-one sulfate, and uracil. Steroid and pyrimidine metabolism pathways were notably active, with peak changes at day 14. Time-dependent patterns showed V-shaped trends for Allobaculum with uracil and cholesterol, while others exhibited inverted V-shaped patterns. Correlation analysis revealed positive associations between Akkermansia and campesterol and negative correlations between Limosilactobacillus and cholesterol (P<0.05). Allobaculum significantly influenced lipid and pyrimidine metabolism (P<0.01), with uracil reduction linked to Ligilactobacillus depletion (P<0.01) (Fig). Conclusion: This study identifies stage-specific microbiota-metabolite networks in the gut-lung axis of PF, revealing interactions that may regulate fibrosis. erj;66/suppl_69/PA1866/F1 F1 F1

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