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Updated: Jan 18, 2026
Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
Multi-Omics Analysis Revealed Characterization of Gastric Microbiome and Metabolome in Helicobacter pylori-Induced
Han Chen1,2, Yan Wang1,2, Yuting Shao1,2
1Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Background:
Several clinical studies have demonstrated that Helicobacter pylori (Hp) infection may exacerbate the progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD); however, the underlying mechanisms remain unclear. This study aims to investigate the characterization of the gastric microbiome and metabolome in relation to the progression of MASLD induced by Hp infection.
Methods:
We established a high-fat diet (HFD) obese mouse model, both with and without Hp infection, to compare alterations in serum and liver metabolic phenotypes. Subsequently, a multi-omics analysis was performed, combining gastric 16S rRNA amplicon sequencing, targeted energy metabolomics, and liver metabolomics sequencing to investigate the correlations among gastric microbiota, energy metabolism, and hepatic metabolism following Hp infection.
Results:
HFD mice infected with Hp exhibited a more severe liver steatosis phenotype compared with Hp-negative controls. Hp infection triggers gastric dysbiosis, resulting in a notable enrichment of the Helicobacter genus, which subsequently becomes the dominant bacterial community. This shift leads to a significant rise in the abundance of other bacteria, such as Enterococcus, Streptococcus, and Staphylococcus, while concurrently reducing beneficial bacterial taxa such as Bifidobacterium. Analysis of bacterial functional enrichment and gastric energy metabolomics consistently reveals elevated glycolytic pathway activity in gastric tissue following Hp infection. Furthermore, liver metabolomics indicate increased activities of both glycolytic and lipid metabolic pathways in the liver. The disturbance of the gastric microbiota-metabolism axis is significantly and positively correlated with the hepatic lactate content and severity of hepatic steatosis and inflammation.
Conclusion:
Hp infection may influence liver metabolism through microbial-metabolic interactions within the gastrohepatic axis, potentially exacerbating the progression of hepatic steatosis. Further studies are necessary to verify these potential causal relationships.
Insights
Helicobacter pylori (Hp) infection worsens metabolic dysfunction-associated steatotic liver disease (MASLD) by altering the gut microbiome and metabolism. This study reveals Hp infection disrupts gastric bacteria, increasing glycolysis and lipid metabolism, which correlates with liver steatosis severity.
Area of Science:
- Gastroenterology and Hepatology
- Microbiology
- Metabolic Diseases
Background:
- Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) progression is potentially exacerbated by Helicobacter pylori (Hp) infection.
- The precise mechanisms linking Hp infection to MASLD remain incompletely understood.
- Investigating the gastric microbiome and metabolome offers insight into Hp-induced MASLD.
Purpose of the Study:
- To characterize gastric microbiome and metabolome alterations in a mouse model of Hp-induced MASLD.
- To explore the relationship between gastric dysbiosis, energy metabolism, and hepatic steatosis.
- To elucidate the gastrohepatic axis in MASLD pathogenesis.
Main Methods:
- A high-fat diet (HFD) induced obese mouse model was utilized, with and without Hp infection.
- Multi-omics analysis included gastric 16S rRNA sequencing, targeted energy metabolomics, and liver metabolomics.
- Correlations between gastric microbiota, energy metabolism, and liver metabolism were investigated.
Main Results:
- Hp infection led to more severe liver steatosis and gastric dysbiosis, enriching Helicobacter and other pathogenic bacteria while reducing beneficial ones.
- Gastric tissue showed elevated glycolytic pathway activity post-Hp infection.
- Liver metabolomics revealed increased glycolytic and lipid metabolic pathway activity, correlating with hepatic steatosis and inflammation.
Conclusions:
- Hp infection may exacerbate hepatic steatosis via microbial-metabolic interactions along the gastrohepatic axis.
- Gastric dysbiosis and altered energy metabolism are implicated in Hp-driven MASLD progression.
- Further research is needed to confirm the causal link between Hp infection and MASLD exacerbation.
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