Fusobacterium Nucleatum Exacerbates Cag Via Mitochondrial Dysfunction And Inflammation

This study investigates the impact of Fusobacterium nucleatum (F.n)-induced mitochondrial damage and inflammation on chronic atrophic gastritis (CAG) in rats. In vivo experiments established a CAG model using MNNG in rats, analyzing F.n's effects on serum inflammatory markers and mitochondrial membrane potential (MMP) of gastric mucosal cells. In vitro studies involved F.n intervention with gastric epithelial cells (GES-1), measuring inflammatory cytokines in cell culture supernatants and MMP changes. In vivo results demonstrated that F.n-treated CAG model rats exhibited elevated serum levels of inflammatory factors (IL-1β, IL-6, TNF-α) and decreased gastric mucosal MMP. In vitro experiments revealed F.n promoted dose-dependent mitochondrial damage and inflammation in gastric mucosal cells. F.n likely exacerbates CAG progression by inducing mitochondrial dysfunction and inflammatory responses in gastric mucosal cells.