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

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). Transcriptomic analysis identified 193 differentially expressed genes (DEGs) between the LPS and LPS+F11.1G groups. Gene Ontology (GO) analysis indicated that DEGs were primarily enriched in cellular response to lipopolysaccharide, inflammatory response, and canonical NF-kappaB signal transduction.