Untitled

Mitochondria play a central role in cellular metabolism, not only by generating ATP through oxidative phosphorylation but also by regulating redox balance, apoptosis, immune responses, and maintaining epithelial barrier integrity, functions particularly critical in energy-demanding tissues such as the intestinal epithelium. Increasing evidence implicates mitochondrial dysfunction as a major factor underlying compromised gut epithelial function and heightened vulnerability to intestinal disease. Our study shows that UV-inactivated Lactiplantibacillus plantarum BGAN8 modulates mitochondrial gene expression and mitochondrial-associated parameters in gut epithelial cells and Caenorhabditis elegans. Transcriptomic profiling of HT29 cells treated with BGAN8 revealed significant upregulation of mitochondrial-encoded genes involved in oxidative phosphorylation, including MT-ND5, MT-CO1, MT-CYB, and MT-ATP6, alongside activation of pathways related to mitochondrial biogenesis, cristae formation, and ATP production. BGAN8 counteracted the adverse effects of kanamycin, an aminoglycoside antibiotic known to impair mitochondrial function. Co-treatment restored mitochondrial gene expression and normalized oxidative stress markers such as SOD1. In C. elegans, BGAN8 administration increased mitochondrial DNA copy number, enhanced expression of genes related to mitochondrial replication (mtss-1), respiration (cox-1), and fusion (fzo-1), increased transmembrane potential, and elevated mitochondrial content as evidenced by GFP-based imaging. Collectively, these findings indicate that UV-inactivated L. plantarum BGAN8 can modulate mitochondrial homeostasis and associated parameters across both cellular and C. elegans models, highlighting the potential of non-viable probiotic bacteria to influence mitochondrial function.