Effect of Helicobacter pylori on gastrointestinal microbiota: a population-based study in Linqu, a high-risk area of gastric cancer

ObjectiveGastrointestinal 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.DesignDeep sequencing of the mi...

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Published inGut Vol. 69; no. 9; pp. 1598 - 1607
Main Authors Guo, Yang, Zhang, Yang, Gerhard, Markus, Gao, Juan-Juan, Mejias-Luque, Raquel, Zhang, Lian, Vieth, Michael, Ma, Jun-Ling, Bajbouj, Monther, Suchanek, Stepan, Liu, Wei-Dong, Ulm, Kurt, Quante, Michael, Li, Zhe-Xuan, Zhou, Tong, Schmid, Roland, Classen, Meinhard, Li, Wen-Qing, You, Wei-Cheng, Pan, Kai-Feng
Format Journal Article
LanguageEnglish
Published England BMJ Publishing Group Ltd and British Society of Gastroenterology 01.09.2020
BMJ Publishing Group LTD
BMJ Publishing Group
SeriesOriginal research
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Abstract ObjectiveGastrointestinal 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.DesignDeep 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.ResultsIn 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.
AbstractList ObjectiveGastrointestinal 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.DesignDeep 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.ResultsIn 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.
ObjectiveGastrointestinal 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.DesignDeep 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.ResultsIn 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.ConclusionH. 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.
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.OBJECTIVEGastrointestinal 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.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.DESIGNDeep 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.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.RESULTSIn 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.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.CONCLUSIONH. 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.
Gastrointestinal microbiota may be involved in associated gastric cancer development. The aim of this study was to explore the possible microbial mechanisms in gastric carcinogenesis and potential dysbiosis arising from infection. 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- treatment, relative to 49 negative subjects. In 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 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 and , , , , were found only in advanced gastric lesion patients, and were absent in normal/superficial gastritis group. Changes in faecal microbiota included increased after successful eradication and more upregulated drug-resistant functional orthologs after failed treatment. infection contributes significantly to gastric microbial dysbiosis that may be involved in carcinogenesis. Successful eradication potentially restores gastric microbiota to a similar status as found in uninfected individuals, and shows beneficial effects on gut microbiota.
Author Zhang, Lian
Bajbouj, Monther
Zhou, Tong
Li, Wen-Qing
Gao, Juan-Juan
Vieth, Michael
Quante, Michael
Guo, Yang
Suchanek, Stepan
Ulm, Kurt
Ma, Jun-Ling
Zhang, Yang
Pan, Kai-Feng
Li, Zhe-Xuan
Mejias-Luque, Raquel
Liu, Wei-Dong
Gerhard, Markus
Schmid, Roland
Classen, Meinhard
You, Wei-Cheng
AuthorAffiliation 4 German Center for Infection Research , Partner Site Munich , Munich , Germany
8 Linqu Public Health Bureau , Linqu , Shandong , China
6 II. Medizinische Klinik, Klinikum Rechts der Isar , Technische Universität München , Munich , Germany
3 Institute of Medical Microbiology, Immunology and Hygiene , Technische Universität München , Munich , Germany
5 Institute of Pathology , Klinikum Bayreuth , Bayreuth , Germany
7 Department of Medicine, 1st Faculty of Medicine , Military University Hospital, Charles University , Prague , Czech Republic
2 PYLOTUM Key joint laboratory for upper GI cancer , Technische Universität München/Peking University Cancer Hospital & Institute , Munich/Beijing , Germany/China
9 Institute of Medical Informatics, Statistics and Epidemiology, Technische Universität München , Munich , Germany
1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology , Peking University Cancer Hospital & Institute , Beijin
AuthorAffiliation_xml – name: 6 II. Medizinische Klinik, Klinikum Rechts der Isar , Technische Universität München , Munich , Germany
– name: 8 Linqu Public Health Bureau , Linqu , Shandong , China
– name: 1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology , Peking University Cancer Hospital & Institute , Beijing , China
– name: 5 Institute of Pathology , Klinikum Bayreuth , Bayreuth , Germany
– name: 2 PYLOTUM Key joint laboratory for upper GI cancer , Technische Universität München/Peking University Cancer Hospital & Institute , Munich/Beijing , Germany/China
– name: 9 Institute of Medical Informatics, Statistics and Epidemiology, Technische Universität München , Munich , Germany
– name: 4 German Center for Infection Research , Partner Site Munich , Munich , Germany
– name: 3 Institute of Medical Microbiology, Immunology and Hygiene , Technische Universität München , Munich , Germany
– name: 7 Department of Medicine, 1st Faculty of Medicine , Military University Hospital, Charles University , Prague , Czech Republic
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  surname: Guo
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  organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China
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  surname: Gao
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  organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China
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  organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China
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  givenname: Wei-Dong
  surname: Liu
  fullname: Liu, Wei-Dong
  organization: Linqu Public Health Bureau, Linqu, Shandong, China
– sequence: 12
  givenname: Kurt
  surname: Ulm
  fullname: Ulm, Kurt
  organization: Institute of Medical Informatics, Statistics and Epidemiology, Technische Universität München, Munich, Germany
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  givenname: Michael
  orcidid: 0000-0002-8497-582X
  surname: Quante
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  organization: PYLOTUM Key joint laboratory for upper GI cancer, Technische Universität München/Peking University Cancer Hospital & Institute, Munich/Beijing, Germany/China
– sequence: 15
  givenname: Tong
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  organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China
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  organization: II. Medizinische Klinik, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany
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  givenname: Wen-Qing
  surname: Li
  fullname: Li, Wen-Qing
  organization: PYLOTUM Key joint laboratory for upper GI cancer, Technische Universität München/Peking University Cancer Hospital & Institute, Munich/Beijing, Germany/China
– sequence: 19
  givenname: Wei-Cheng
  surname: You
  fullname: You, Wei-Cheng
  email: weichengyou@yahoo.com
  organization: PYLOTUM Key joint laboratory for upper GI cancer, Technische Universität München/Peking University Cancer Hospital & Institute, Munich/Beijing, Germany/China
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  surname: Pan
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  email: pankaifeng2002@yahoo.com
  organization: PYLOTUM Key joint laboratory for upper GI cancer, Technische Universität München/Peking University Cancer Hospital & Institute, Munich/Beijing, Germany/China
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31857433$$D View this record in MEDLINE/PubMed
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Issue 9
Keywords bacterial interactions
gastric diseases
gastric pre-cancer
helicobacter pylori - treatment
Language English
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Snippet ObjectiveGastrointestinal microbiota may be involved in Helicobacter pylori-associated gastric cancer development. The aim of this study was to explore the...
Gastrointestinal microbiota may be involved in associated gastric cancer development. The aim of this study was to explore the possible microbial mechanisms in...
Gastrointestinal microbiota may be involved in Helicobacter pylori-associated gastric cancer development. The aim of this study was to explore the possible...
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SubjectTerms Age
Anti-Bacterial Agents - therapeutic use
Antibiotics
Bacteria
bacterial interactions
Biopsy
Biopsy - methods
Carcinogenesis
Deoxyribonucleic acid
DNA
Drug resistance
Dysbacteriosis
Dysbiosis - diagnosis
Dysbiosis - microbiology
Dysplasia
Endoscopy
Epidemiology
Feces - microbiology
Female
Gastric cancer
gastric diseases
Gastric Mucosa - microbiology
Gastric Mucosa - pathology
gastric pre-cancer
Gastritis
Gastritis, Atrophic - microbiology
Gastritis, Atrophic - pathology
Gastrointestinal Microbiome - genetics
Gut Microbiota
Helicobacter Infections - drug therapy
Helicobacter Infections - pathology
Helicobacter pylori
Helicobacter pylori - isolation & purification
Helicobacter pylori - pathogenicity
helicobacter pylori - treatment
Humans
Intestinal microflora
Intestine
Laboratories
Male
Metabolism
Metaplasia
Metaplasia - microbiology
Metaplasia - pathology
Microbial Interactions
Microbiota
Middle Aged
Mucosa
Population studies
Population-based studies
Prevention
RNA, Ribosomal, 16S - isolation & purification
rRNA 16S
Stomach Neoplasms - microbiology
Stomach Neoplasms - pathology
Studies
Taxonomy
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Title Effect of Helicobacter pylori on gastrointestinal microbiota: a population-based study in Linqu, a high-risk area of gastric cancer
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Volume 69
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