Cancer biology & medicine · 2026
Dietary nitrate drives gastritis by modulating gastric microbiota and metabolites.
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Jiang Lanping, Li Tianhui, Wu Jiayu, Lau Harry Cheuk Hay, Wong Chi Chun, Zhou Xingyu, Cheung Alvin Ho Kwan, Wei Qinyao, Ren Jing, Zhang Xiang, Li Qing, Nie Yongzhan, Yu Jun
Аннотация
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.
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.