Patients with concurrent Helicobacter pylori infection and small intestinal bacterial overgrowth (SIBO) represent a clinically challenging subgroup, often experiencing refractory gastrointestinal symptoms and diminished treatment responses. Current evidence indicates that individuals infected with H. pylori may related SIBO as a comorbidity; however, the synergistic effects of these conditions on gut ecosystem homeostasis remain poorly understood. To address this knowledge gap, we employed a dual-omics approach that combined shotgun metagenomic sequencing with liquid chromatography-mass spectrometry (LC-MS) metabolomic profiling. This methodology allowed for a comprehensive mapping of microbial community structures, including species-level taxonomy and functional pathways, as well as host-microbiota co-metabolism signatures in fecal samples.
Patients presenting with concurrent Helicobacter pylori infection and small intestinal bacterial overgrowth (SIBO) constitute a clinically challenging subgroup characterized by refractory gastrointestinal symptoms and diminished responses to standard therapeutic interventions. Current evidence supports an association between H. pylori infection and an increased prevalence of SIBO as a comorbidity. However, the synergistic effects of these two conditions on the fundamental mechanisms governing gut ecosystem homeostasis - particularly concerning microbial community dynamics, functional metabolic output, and host-microbial interactions - remain poorly understood, representing a significant knowledge gap. To systematically address this gap and elucidate the complex interplay, we implemented an integrated dual-omics analytical approach. This methodology combined shotgun metagenomic sequencing of fecal samples with liquid chromatography-mass spectrometry (LC-MS) metabolomic profiling. This powerful combination enables a comprehensive mapping of the gut ecosystem by simultaneously characterizing: Host-Microbiota Co-Metabolism Signatures: Revealing the metabolic landscape through the detection and quantification of metabolites derived from microbial activity, host metabolism, and crucially, their interactions (co-metabolism) within the fecal metabolome. This multimodal strategy offers an unprecedented, holistic view of the perturbations induced by the co-occurrence of H. pylori infection and SIBO, moving beyond singular aspects to capture the integrated functional and compositional state of the gut ecosystem.
Study Type
OBSERVATIONAL
Enrollment
42
Participants underwent the 13C-urea breath test following a standardized protocol to detect active Helicobacter pylori (H. pylori) infection. After an overnight fast (≥8 hours), baseline breath samples were collected by exhaling gently through a straw. Participants then ingested 75 mg of 13C-labeled urea dissolved in 50 mL of citric acid solution to delay gastric emptying and maximize urease exposure. A second breath sample was collected 30 minutes post-ingestion using identical procedures.
Participants underwent a standardized hydrogen-methane breath test to evaluate for small intestinal bacterial overgrowth (SIBO) or carbohydrate malabsorption. After a 12-hour overnight fast, baseline breath samples were collected via controlled end-expiratory exhalation. Participants then ingested a substrate solution.
Zhongshan Hospital (Xiamen), Fudan University
Xiamen, Fujian, China
13C-Urea Breath Test
The 13C-Urea Breath Test (13C-UBT) is a non-invasive, highly specific diagnostic assay used to detect active Helicobacter pylori (H. pylori) infection in the gastric mucosa. It leverages the bacterium's unique enzymatic activity-urease production-to metabolize ingested labeled urea, resulting in measurable changes in exhaled breath CO₂ isotopic composition.
Time frame: day 0, Patient baseline levels at enrollment
Hydrogen-Methane Breath Test
The Hydrogen-Methane Breath Test (HMBT) is a non-invasive, gold-standard diagnostic tool for detecting small intestinal bacterial overgrowth (SIBO) and carbohydrate malabsorption disorders . It quantifies microbial fermentation activity in the gut by measuring gaseous metabolic end-products (H₂ and CH₄) in exhaled breath following substrate administration.
Time frame: day 0, Patient baseline levels at enrollment
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