Effect of Helicobacter pylori on gastrointestinal microbiota: a population-based study in Linqu, a high-risk area of gastric cancer
Effect of Helicobacter pylori on gastrointestinal microbiota: a population-based study in Linqu, a high-risk area of gastric cancer
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幽门螺杆菌对胃肠道微生物群的影响：胃癌高发区临朐县的人群研究
DOI：
10.1136/gutjnl-2019-319696
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发表时间：
2020-09-01
期刊：
影响因子：
24.5
通讯作者：
Pan, Kai-Feng
中科院分区：
文献类型：
--
作者：
Guo, Yang;Zhang, Yang;Pan, Kai-Feng
目的胃肠道菌群可能参与幽门螺杆菌相关性胃癌的发生。本研究的目的是探讨胃癌发生过程中可能的微生物学机制以及H。幽门感染设计使用微生物16 S核糖体RNA基因的深度测序来研究58名成功的抗H抗体受试者和57名失败的抗H抗体受试者的配对胃活检和粪便样本的变化。pylori治疗，相对于49 H. pylori阴性受试者。结果在H. pylori阳性者在根除后，其丰富度和Shannon指数均显著升高（均P<0.001），与阴性者无差异（丰富度p=0.493，Shannon指数p=0.420）。差异类群分析确定了18个显着改变后根除胃属。将这些属组合成微生物生态失调指数揭示了H。pylori阳性粘膜与晚期胃病变（慢性萎缩性胃炎和肠上皮化生/异型增生）相关，可通过根除逆转。幽门螺杆菌与梭杆菌、奈瑟氏菌、普雷沃菌、韦荣球菌、罗氏菌之间的相互作用仅在进展期胃病变组中存在，而在正常/浅表性胃炎组中不存在。粪便微生物群的变化包括成功的H.幽门螺杆菌根除和治疗失败后更多的上调耐药功能性直系同源物。结论H.幽门螺杆菌感染对胃微生物生态失调有重要作用，而胃微生物生态失调可能与癌的发生有关。成功的H。幽门螺杆菌根除可能使胃微生物群恢复到与未感染个体相似的状态，并显示出对肠道微生物群的有益作用。
Objective Gastrointestinal microbiota may be involved in Helicobacter pylori-associated gastric cancer development. The aim of this study was to explore the possible microbial mechanisms in gastric carcinogenesis and potential dysbiosis arising from H. pylori infection. Design Deep sequencing of the microbial 16S ribosomal RNA gene was used to investigate alterations in paired gastric biopsies and stool samples in 58 subjects with successful and 57 subjects with failed anti-H. pylori treatment, relative to 49 H. pylori negative subjects. Results In H. pylori positive subjects, richness and Shannon indexes increased significantly (both p<0.001) after successful eradication and showed no difference to those of negative subjects (p=0.493 for richness and p=0.420 for Shannon index). Differential taxa analysis identified 18 significantly altered gastric genera after eradication. The combination of these genera into a Microbial Dysbiosis Index revealed that the dysbiotic microbiota in H. pylori positive mucosa was associated with advanced gastric lesions (chronic atrophic gastritis and intestinal metaplasia/dysplasia) and could be reversed by eradication. Strong coexcluding interactions between Helicobacter and Fusobacterium, Neisseria, Prevotella, Veillonella, Rothia were found only in advanced gastric lesion patients, and were absent in normal/superficial gastritis group. Changes in faecal microbiota included increased Bifidobacterium after successful H. pylori eradication and more upregulated drug-resistant functional orthologs after failed treatment. Conclusion H. pylori infection contributes significantly to gastric microbial dysbiosis that may be involved in carcinogenesis. Successful H. pylori eradication potentially restores gastric microbiota to a similar status as found in uninfected individuals, and shows beneficial effects on gut microbiota.