Investigating the Mechanism of Ultrasonic Lysis of Enterococcus faecium F11.1G in Repairing LPS-Induced Inflammatory Damage in IECs via LC-MS

Lipopolysaccharide (LPS)-induced damage to the intestinal epithelial barrier is pivotal in intestinal inflammation pathogenesis. While lactic acid bacteria (LAB) and their derivatives show probiotic promise, the mechanisms, particularly those of their intracellular metabolites, remain unclear. This study aimed to investigate the repair effects and molecular mechanisms of ultrasonic disruption-treated Enterococcus faecium F11.1G (F11.1G) on LPS-induced inflammatory damage in intestinal epithelial cells (IECs). IECs were divided into three groups: NC group (untreated control), LPS group (treated with 5 μg/mL LPS for 6 h), and LPS+F11.1G group (treated with 5 μg/mL LPS for 6 h, followed by 10⁸ CFU/mL F11.1G for 6 h). Metabolomics identified 46 differentially altered metabolites (DAMs) between the LPS and LPS+F11.1G groups (Adenosine, Palmitoyl ethanolamide (PEA) etc. ), with KEGG enrichment in purine metabolism and the endocannabinoid system. Spearman correlation analysis revealed positive correlations between proinflammatory genes and endogenous protective metabolites like Adenosine and PEA, while showing negative correlations with multiple purine metabolites.