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Gastrointestinal microbiome and Helicobacter pylori:Eradicate,leave it as it is,or take a personalized benefit-risk approach?

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World Journal of Gastroenterology 2022年第7期28卷 766-774页

作者： Stanislav Sitkin Leonid Lazebnik Elena Avalueva Svetlana Kononova Timur Vakhitov Department of Internal Diseases Gastroenterology and DieteticsNorth-Western State Medical University Named After I.I.MechnikovSt.Petersburg 191015Russia Non-Infectious Disease Metabolomics Group Institute of Experimental MedicineSt.Petersburg 197376Russia Epigenetics and Metagenomics Group Institute of Perinatology and PediatricsAlmazov National Medical Research CentreSt.Petersburg 197341Russia Department of Outpatient Therapy A.I.Yevdokimov Moscow State University of Medicine and DentistryMoscow 127473Russia Institute of Protein Research Russian Academy of SciencesPushchinoMoscow region 142290Russia

Helicobacter pylori(***)is generally regarded as a human pathogen and a class 1 carcinogen,etiologically related to gastric and duodenal ulcers,gastric cancer,and mucosa-associated lymphoid tissue ***,*** can also be regarded as a commensal *** other pathogenic/opportunistic bacteria,*** colonization in infancy is facilitated by T helper type 2 immunity and leads to the development of immune *** gastric mucin glycans,which are an important part of the innate and adaptive immune system,mediate the adhesion of *** to the surface of the gastric epithelium,contributing to successful *** may have beneficial effects on the host by regulating gastrointestinal(GI)microbiota and protecting against some allergic and autoimmune disorders and inflammatory bowel *** potential protective role against inflammatory bowel disease may be related to both modulation of the gut microbiota and the immunomodulatory properties of *** inverse association between *** and some potentially proinflammatory and/or procarcinogenic bacteria may suggest it regulates the GI *** of *** can cause various adverse effects and alter the GI microbiota,leading to short-term or long-term ***,studies have shown that gastric Actinobacteria decrease after *** eradication,Proteobacteria increase during short-term follow-up and then return to baseline levels,and Enterobacteriaceae and Enterococcus increase in the short-term and interim *** gastric mucosal bacteria(Actinomyces,Granulicatella,Parvimonas,Peptostreptococcus,Prevotella,Rothia,Streptococcus,Rhodococcus,and Lactobacillus)may contribute to precancerous gastric lesions and cancer itself after *** *** eradication can also lead to dysbiosis of the gut microbiota,with increased Proteobacteria and decreased Bacteroidetes and *** increase in gut Proteobacteria may c

关键词： Helicobacter pylori Eradication Gastrointestinal microbiota Dysbiosis fucosylated glycan Inflammatory bowel disease

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