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Original Article | Open Access

Dietary nitrate drives gastritis by modulating gastric microbiota and metabolites

Lanping Jiang1,*, Tianhui Li1,*, Jiayu Wu1,*, Harry Cheuk Hay Lau1,*, Chi Chun Wong1, Xingyu Zhou1, Alvin Ho Kwan Cheung2, Qinyao Wei1, Jing Ren3, Xiang Zhang1, Qing Li1, Yongzhan Nie4, Jun Yu1 ( )
Institute of Digestive Disease and Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China
Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Hong Kong SAR, China
Department of Anaesthesia and Intensive Care and Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong SAR, China
Department of Gastroenterology, State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and National Clinical Research Center for Digestive Diseases, Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi’an 710032, China

*These authors contributed equally to this work.

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Abstract

Objective

Dietary nitrate has been increasingly recognized as a potential carcinogen associated with gastritis. In this study the mechanistic role of a high-nitrate diet (NaD) in driving gastritis was elucidated with a focus on modulation of the gastric microbiota composition and metabolomic profiles.

Methods

Animals were randomly assigned to two dietary intervention groups using a C57BL/6 mouse model: a NaD containing 7.5% nitrate; or a standard normal diet (ND). Gastric microbiota composition was characterized based on full-length 16S rRNA sequencing and gastric metabolite profiles were analyzed using high-performance liquid chromatography-mass spectrometry (HPLC/MS). Finally, the roles of the microbiome and metabolites in gastritis development were validated using the human gastric epithelial cell line (GES-1), as well as conventional and germ-free mouse models.

Results

NaD induced gastritis in conventional mice compared to ND-fed mice. In addition, NaD incited the infiltration of macrophages and neutrophils with elevated levels of inflammatory cytokine genes (IL-17a, Ccl20, Cxcl5, IL-6, and Ccl2). A significant shift in the composition of the gastric microbiota occurred with an increase in pathogenic bacteria (Enterococcus gallinarum, Prevotella timonensis, and Mycobacterium gordona) and a decrease in probiotics (Roseburia hominis, Clostriduim scindens, and Faecalibacterium prausnitzii). Furthermore, NaD induced alterations in the metabolic profile, marked by an elevated level of 5-hydroxyindoleacetate (5-HIAA), a key downstream metabolite of the tryptophan metabolic pathway. Notably, 5-HIAA also upregulated the levels of inflammatory cytokines in the human gastric epithelial GES-1 cell line. In addition, both E. gallinarum colonization and 5-HIAA exposure significantly increased inflammatory responses in conventional and germ-free mouse models.

Conclusions

NaD drives gastritis in mice by inducing gastric microbial dysbiosis and metabolomic dysregulation with elevated 5-HIAA.

Keywords

Nitrate dietgastritisEnterococcus gallinarum5-HIAAgerm-free mouse

Electronic Supplementary Material

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Cancer Biology & Medicine
Volume 23 Issue 5,
May 2026
Pages 717-736
DOI: 10.20892/j.issn.2095-3941.2025.0679

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Cite this article:
Jiang L, Li T, Wu J, et al. Dietary nitrate drives gastritis by modulating gastric microbiota and metabolites. Cancer Biology & Medicine, 2026, 23(5): 717-736. https://doi.org/10.20892/j.issn.2095-3941.2025.0679

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Received: 11 December 2025
Accepted: 25 February 2026
Published: 25 April 2026
©2026 The Authors.

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