NAD+激酶
代谢物
肠道菌群
胃炎
微生物群
胃粘膜
炎症
细胞因子
生物
代谢组学
幽门螺杆菌
药理学
毛螺菌科
促炎细胞因子
胃
化学
免疫学
微生物学
失调
生物化学
内科学
亚硝酸盐
TLR4型
医学
代谢途径
慢性胃炎
细菌
下调和上调
螺杆菌
作者
Lanping Jiang,Tianhui Li,Jiayu Wu,Harry Cheuk Hay Lau,Chi Chun Wong,Xingyu Zhou,Alvin Ho Kwan Cheung,Qinyao Wei,Jing Ren,Xiang Zhang,Qi Li,Yongzhan Nie,Jun Yu
标识
DOI:10.20892/j.issn.2095-3941.2025.0679
摘要
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: 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.
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