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Mechanisms of action of bile acids in pediatric gastroesophageal reflux: Exploration through non-targeted and targeted metabolomics methods

ABSTRACT:

Purpose: To investigate the pathogenesis of pediatric bile reflux gastritis (BRG) using non-targeted and targeted metabolomics analyses of the changes and content differences of bile acids (BAs) in gastric juice. Methods: Data from 25 pediatric BRG patients treated at Jinhua Maternal and Child Health Care Hospital between May 2022 and August 2023 were retrospectively analyzed. Twenty-five patients with gastritis without bile reflux and 25 healthy controls were selected for the comparison of total bile acids (TBA) levels of gastric juice and peripheral blood and the identification of differential metabolites. The correlations of gastric juice and peripheral blood TBA levels with the clinical characteristics of the pediatric BRG patients were analyzed. Receiver operating characteristic (ROC) curves were plotted to determine the area under ROC curve (AUC), sensitivity, and specificity of TBA in diagnosing BRG. Results: Identification and quantitative metabolomics revealed that the top 10 differential metabolites of gastric juice between the BRG and healthy control groups were fatty acids, phospholipids, 23-carbon compounds, amines, vitamins, steroids, peptide hormones, monosaccharides, polyketides, and non-ribosomal peptides. This indicated that glycerophospholipid metabolism, prodigiosin biosynthesis, lysine degradation, glycerolipid metabolism, and primary BA biosynthesis were the most relevant pathways. Differential metabolites were primarily concentrated in the T helper 17 (Th17) cell differentiation pathway (P < 0.05, effect value>0.1). Conclusion: The metabolites and metabolic pathways identified in different groups will aid in elucidating the pathogenic mechanisms underlying pediatric BRG. Gastric juice and peripheral blood TBA levels showed a trend of aberrant expression in pediatric BRG patients, potentially guiding clinical diagnosis.

INSTRUMENT(S): Liquid Chromatography MS - alternating - reverse-phase

PROVIDER: MTBLS13450 | MetaboLights | 2025-12-04

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13450_LC-MS_alternating_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13450_LC-MS_alternating_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	s_MTBLS13450.txt	Txt

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Project description:Helicobacter pylori (H. pylori) infection induces chronic infla mmation of the gastric mucosa. There is a close relationship between Th1 7/Treg cell imbalance and adverse outcomes associated with H. pylori inf ection. The differentiation and development of both Th17 and Treg cells r equire the regulatory involvement of TGF-β. However, the regulatory role of the TGF-β signaling pathway in H. pylori-induced gastritis remains un clear. The aim of this study was to investigate the impact of H. pylori infe ction on the expression of TGF-β pathway proteins in patients with chroni In reviewc gastritis, as well as changes in Th17 and Treg cells and their cytokine ex pression levels. In this study, gastric mucosal proteomic analysis revealed that differentially expressed proteins were enriched in signaling pathway s such as TGF-β, MAPK, and Th17. Experiments demonstrated that TGF- β1 and TAK1 mRNA levels, along with their protein expression, were inc reased in both the peripheral blood and gastric mucosa of H. pylori-infect ed gastritis patients. Compared to the negative control group, H. pylori-in fected gastritis patients showed elevated levels of Th17 and Treg cell tran scription factors (RORγt and Foxp3 mRNA) in peripheral blood and gastri c mucosa, as well as increased IL-17 and Foxp3 protein expression in gas tric mucosa and elevated IL-17 and IL-10 levels in peripheral blood. Ani mal experiments revealed a decreased Th17/Treg ratio in H. pylori-infecte d gastritis mice. We hypothesize that H. pylori infection may participate i n gastric mucosal inflammatory responses by activating the TGF-β signali ng pathway and interacting with the immune balance between Th17 and T reg cells during inflammation. These findings provide new strategies for t he prevention and treatment of H. pylori-induced gastritis. This translatio n maintains medical accuracy while ensuring fluency and adherence to sta ndard scientific writing conventions. Let me know if you'd like any refine ments!

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Mechanisms of action of bile acids in pediatric gastroesophageal reflux: Exploration through non-targeted and targeted metabolomics methods

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