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Abstract：
BACKGROUND: Helicobacter pylori (H. pylori) infection is closely associated with gastrointestinal diseases. Our preliminary studies have indicated that H. pylori infection had a significant impact on the mucosal microbiome structure in patients with gastric ulcer (GU) or duodenal ulcer (DU).
OBJECTIVE: To investigate the contributions of H. pylori infection and the mucosal microbiome to the pathogenesis and progression of ulcerative diseases.
METHODS: Patients with H. pylori infection and either GU or DU, and healthy individuals without H. pylori infection were included. Gastric or duodenal mucosal samples was obtained and subjected to metagenomic sequencing. The compositions of the microbial communities and their metabolic functions in the mucosal tissues were analyzed.
RESULTS: Compared with that in the healthy individuals, the gastric mucosal microbiota in the H. pylori-positive patients with GU was dominated by H. pylori, with significantly reduced biodiversity. The intergroup differential functions, which were enriched in the H. pylori-positive GU patients, were all derived from H. pylori, particularly those concerning transfer RNA queuosine-modification and the synthesis of demethylmenaquinones or menaquinones. A significant enrichment of the uibE gene was detected in the synthesis pathway. There was no significant difference in microbial diversity between the H. pylori-positive DU patients and healthy controls.
CONCLUSIONS: H. pylori infection significantly alters the gastric microbiota structure, diversity, and biological functions, which may be important contributing factors for GU.
OBJECTIVE: To investigate the contributions of H. pylori infection and the mucosal microbiome to the pathogenesis and progression of ulcerative diseases.
METHODS: Patients with H. pylori infection and either GU or DU, and healthy individuals without H. pylori infection were included. Gastric or duodenal mucosal samples was obtained and subjected to metagenomic sequencing. The compositions of the microbial communities and their metabolic functions in the mucosal tissues were analyzed.
RESULTS: Compared with that in the healthy individuals, the gastric mucosal microbiota in the H. pylori-positive patients with GU was dominated by H. pylori, with significantly reduced biodiversity. The intergroup differential functions, which were enriched in the H. pylori-positive GU patients, were all derived from H. pylori, particularly those concerning transfer RNA queuosine-modification and the synthesis of demethylmenaquinones or menaquinones. A significant enrichment of the uibE gene was detected in the synthesis pathway. There was no significant difference in microbial diversity between the H. pylori-positive DU patients and healthy controls.
CONCLUSIONS: H. pylori infection significantly alters the gastric microbiota structure, diversity, and biological functions, which may be important contributing factors for GU.
摘要：
背景：幽门螺杆菌(H.幽门螺杆菌)感染与胃肠道疾病密切相关。我们的初步研究表明，幽门螺杆菌感染对胃溃疡（GU）或十二指肠溃疡（DU）患者的粘膜微生物组结构有重大影响。
目的：探讨幽门螺杆菌感染和黏膜微生物群对溃疡性疾病发病及进展的影响。
方法：幽门螺杆菌感染和GU或DU的患者，和没有幽门螺杆菌感染的健康个体被包括在内。获得胃或十二指肠粘膜样品并进行宏基因组测序。分析了微生物群落的组成及其在粘膜组织中的代谢功能。
结果：与健康个体相比，幽门螺杆菌阳性GU患者的胃粘膜微生物群以幽门螺杆菌为主，生物多样性显著减少。组间微分函数，富含幽门螺杆菌阳性GU患者，都来自幽门螺杆菌，特别是那些涉及转移RNA的糖苷修饰和去甲基甲基甲萘醌或甲萘醌的合成。在合成途径中检测到uibE基因的显著富集。幽门螺杆菌阳性DU患者和健康对照组之间的微生物多样性没有显着差异。
结论：H.幽门螺杆菌感染显著改变了胃微生物群结构，多样性,和生物学功能，这可能是GU的重要促成因素。
目的：探讨幽门螺杆菌感染和黏膜微生物群对溃疡性疾病发病及进展的影响。
方法：幽门螺杆菌感染和GU或DU的患者，和没有幽门螺杆菌感染的健康个体被包括在内。获得胃或十二指肠粘膜样品并进行宏基因组测序。分析了微生物群落的组成及其在粘膜组织中的代谢功能。
结果：与健康个体相比，幽门螺杆菌阳性GU患者的胃粘膜微生物群以幽门螺杆菌为主，生物多样性显著减少。组间微分函数，富含幽门螺杆菌阳性GU患者，都来自幽门螺杆菌，特别是那些涉及转移RNA的糖苷修饰和去甲基甲基甲萘醌或甲萘醌的合成。在合成途径中检测到uibE基因的显著富集。幽门螺杆菌阳性DU患者和健康对照组之间的微生物多样性没有显着差异。
结论：H.幽门螺杆菌感染显著改变了胃微生物群结构，多样性,和生物学功能，这可能是GU的重要促成因素。
