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

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). 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. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed enrichment in NF-kappaB (NF-κB) signaling pathway and MAPK signaling pathway. The protein-protein interaction (PPI) network identified key genes including IL1B, TNF, CXCL8, RELB, FOS, TNFAIP3, NFKBIA, and MMP9 etc..