Ma Yumei, Jiang Jianming, Yang Zhufeng, Li Yongzhang, Bai Haiyan, Liu Zongxiu, Zhang Shuo, Zhi Zheng, Yang Qian
Department of Reserch Center, Hebei Province Hospital of Chinese Medicine, 389 Zhongshan East Road, Shijiazhuang, 050011, Hebei, China.
Hebei Key Laboratory of Integrated Chinese and Western Medicine for Gastroenterology Research, 389 Zhongshan East Road, Shijiazhuang, 050011, Hebei, China.
J Transl Med. 2025 May 13;23(1):537. doi: 10.1186/s12967-025-06458-7.
Chronic atrophic gastritis (CAG) is related to the body's microbial and metabolic systems. Combined studies of microbiome and metabolomics can clarify the mechanisms of disease occurrence and progression. We used 16S rRNA sequencing, metagenomics sequencing and metabolomics sequencing to depict the landscapes of bacterium and metabolites, construct correlation networks of different bacterium and metabolites describe potential pathogenic mechanisms of chronic atrophic gastritis.
The gastric juices of 30 non-atrophic gastritis (NAG) patients and 30 CAG patients were collected. Gastric microflora was analyzed by 16S rRNA sequencing and metagenomics sequencing. Gastric metabolites were analyzed by LC-MS analysis. Different bioinformatics methods were used to analyze the data of microbiome and metabolome, and to analyze the relationship between them.
In atrophic gastritis, bacteria diversity decreased. The genera with a mean decrease in Gini greater than 1.5 included peptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides. KEGG pathway included renal cell carcinoma, proximal tubule bicarbonate reclamation, citrate cycle and aldosterone synthesis and secretion with significant enrichment of differential metabolites. Peptostreptococcus, fusobacterium, prevotella and sphingomonas were in pivot positions of the correlation network of differential metabolites and differential bacterium. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism were enriched in chronic atrophic gastritis based on the metagenomic sequencing data.
Peptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides were the essential features that distinguish atrophic gastritis from non-atrophic gastritis, and caused disease by altering various metabolic pathways. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism may be related to the occurrence and progression of CAG.
慢性萎缩性胃炎（CAG）与人体微生物和代谢系统相关。微生物组学和代谢组学的联合研究能够阐明疾病发生和发展的机制。我们运用16S rRNA测序、宏基因组测序和代谢组学测序来描绘细菌和代谢物图谱，构建不同细菌与代谢物的关联网络，以描述慢性萎缩性胃炎的潜在致病机制。
收集30例非萎缩性胃炎（NAG）患者和30例CAG患者的胃液。通过16S rRNA测序和宏基因组测序分析胃微生物群。通过液相色谱 - 质谱分析（LC-MS分析）胃代谢物。采用不同的生物信息学方法分析微生物组和代谢组数据，并分析它们之间的关系。
在萎缩性胃炎中，细菌多样性降低。基尼系数平均下降大于1.5的菌属包括消化链球菌属、梭杆菌属、普雷沃菌属、鞘氨醇单胞菌属和拟杆菌属。KEGG通路包括肾细胞癌、近端小管碳酸氢盐重吸收、柠檬酸循环以及醛固酮合成和分泌，差异代谢物有显著富集。消化链球菌属、梭杆菌属、普雷沃菌属和鞘氨醇单胞菌属处于差异代谢物与差异细菌关联网络的枢纽位置。基于宏基因组测序数据，病毒致癌、甘氨酸丝氨酸和苏氨酸代谢、RNA聚合酶、半乳糖代谢和视黄醇代谢在慢性萎缩性胃炎中富集。
消化链球菌属、梭杆菌属、普雷沃菌属、鞘氨醇单胞菌属和拟杆菌属是区分萎缩性胃炎与非萎缩性胃炎的关键特征，并通过改变各种代谢途径引发疾病。病毒致癌、甘氨酸丝氨酸和苏氨酸代谢、RNA聚合酶、半乳糖代谢和视黄醇代谢可能与CAG 的发生和发展有关。
