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Updated: Jun 5, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Fusobacterium nucleatum exacerbates chronic atrophic gastritis in rats via mitochondrial dysfunction and inflammatory
Peixun Zhao1,2, Yiyang Fan1,2, Haohan Liu1,2
1Department of Cariology and Endodontics, First Affiliated Hospital of Xinjiang Medical University (The Affiliated Stomatology Hospital of Xinjiang Medical University), Urumqi, China.
Background:
Chronic atrophic gastritis (CAG) is a premalignant condition with limited therapeutic strategies. The role of the oral pathogen Fusobacterium nucleatum (F. nucleatum), associated with gastrointestinal carcinogenesis, in CAG remains unclear.
Methods:
This study investigated whether F. nucleatum aggravates gastric mucosal injury through inflammation and mitochondrial dysfunction in CAG. A rat model of CAG was induced using N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) for 10 weeks, combined with oral gavage of F. nucleatum. Gastric pathology, bacterial colonization, serum cytokine levels, and mitochondrial membrane potential were evaluated. In vitro, human gastric epithelial cells (GES-1) were treated with MNNG and co-cultured with F. nucleatum at multiplicities of infection (MOI) of 50, 100, or 150. Cytokine concentrations in cell culture supernatants were quantified using corresponding human enzyme-linked immunosorbent assay kits. Mitochondrial membrane potential was assessed via flow cytometry.
Results:
F. nucleatum colonized gastric tissues and intensified MNNG-induced injury, including rugal flattening, glandular atrophy, intestinal metaplasia, and inflammatory cell infiltration. It significantly increased pro-inflammatory cytokine levels and further decreased mitochondrial membrane potential. In GES-1 cells, F. nucleatum dose-dependently elevated secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) and impaired mitochondrial function.
Conclusions:
F. nucleatum exacerbates CAG by promoting gastric inflammation and mitochondrial dysfunction. These findings may underscore the microbiota-mitochondria axis as a potential therapeutic target to prevent CAG progression.
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