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 in | Gut Vol. 69; no. 9; pp. 1598 - 1607 |
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Main Authors | , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
BMJ Publishing Group Ltd and British Society of Gastroenterology
01.09.2020
BMJ Publishing Group LTD BMJ Publishing Group |
Series | Original research |
Subjects | |
Online Access | Get full text |
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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. |
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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 |
Author_xml | – sequence: 1 givenname: Yang surname: Guo fullname: Guo, Yang organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China – sequence: 2 givenname: Yang orcidid: 0000-0002-8209-819X surname: Zhang fullname: Zhang, Yang organization: PYLOTUM Key joint laboratory for upper GI cancer, Technische Universität München/Peking University Cancer Hospital & Institute, Munich/Beijing, Germany/China – sequence: 3 givenname: Markus surname: Gerhard fullname: Gerhard, Markus organization: German Center for Infection Research, Partner Site Munich, Munich, Germany – sequence: 4 givenname: Juan-Juan surname: Gao fullname: Gao, Juan-Juan organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China – sequence: 5 givenname: Raquel surname: Mejias-Luque fullname: Mejias-Luque, Raquel organization: German Center for Infection Research, Partner Site Munich, Munich, Germany – sequence: 6 givenname: Lian surname: Zhang fullname: Zhang, Lian organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China – sequence: 7 givenname: Michael surname: Vieth fullname: Vieth, Michael organization: Institute of Pathology, Klinikum Bayreuth, Bayreuth, Germany – sequence: 8 givenname: Jun-Ling surname: Ma fullname: Ma, Jun-Ling organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China – sequence: 9 givenname: Monther surname: Bajbouj fullname: Bajbouj, Monther organization: II. Medizinische Klinik, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany – sequence: 10 givenname: Stepan surname: Suchanek fullname: Suchanek, Stepan organization: Department of Medicine, 1st Faculty of Medicine, Military University Hospital, Charles University, Prague, Czech Republic – sequence: 11 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 – sequence: 13 givenname: Michael orcidid: 0000-0002-8497-582X surname: Quante fullname: Quante, Michael organization: II. Medizinische Klinik, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany – sequence: 14 givenname: Zhe-Xuan surname: Li fullname: Li, Zhe-Xuan 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 surname: Zhou fullname: Zhou, Tong organization: Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China – sequence: 16 givenname: Roland surname: Schmid fullname: Schmid, Roland organization: II. Medizinische Klinik, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany – sequence: 17 givenname: Meinhard surname: Classen fullname: Classen, Meinhard organization: II. Medizinische Klinik, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany – sequence: 18 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 – sequence: 20 givenname: Kai-Feng surname: Pan fullname: Pan, Kai-Feng 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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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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