To investigate the intricate interactions among immunity, metabolism, and the microbiome in acute pancreatitis (AP) through a comprehensive multi-omics analysis.
Approach:
Key Findings:
Identified 4,776 DEGs, including 409 immune-related genes significantly enriched in the NF-κB, IL-17, and cytokine-cytokine receptor interaction pathways.
Detected 296 DEMs with significant alterations in amino acid and lipid metabolism, with 9 metabolites showing potential discriminatory value (AUC > 0.75), including xanthine, homocarnosine, and tetradecanedioic acid.
Revealed significant microbial compositional changes, including enrichment of pro-inflammatory taxa such as Escherichia coli and Streptococcus anginosus, and depletion of SCFA-producing commensals like Faecalibacterium prausnitzii and Blautia wexlerae.
Established 215 significant correlations between host genes, metabolites, and microbes, highlighting key interaction hubs.
Identified candidate biomarkers including Lachnospira pectinoschiza, Megamonas funiformis, and SRGN, showing promising classification performance (AUC = 0.951).
Interpretation:
The study provides a systems-level characterization of immune, metabolic, and microbial alterations in AP.
Limitations:
The study involved a small cohort size, which may limit the generalizability of the findings.
Findings require validation in larger, independent cohorts to confirm the results.
Conclusion:
The identified molecular signatures and cross-omics interaction networks enhance understanding of AP pathogenesis.
