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Helicobacter pylori ( H. 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 lymphoma. However, H. pylori can also be regarded as a commensal symbiont. Unlike other pathogenic/ opportunistic bacteria, H. pylori colonization in infancy is facilitated by T helper type 2 immunity and leads to the development of immune tolerance. Fucosylated gastric mucin glycans, which are an important part of the innate and adaptive immune system, mediate the adhesion of H. pylori o the surface of the gastric epithelium, contributing to successful colonization. H. pylori may have beneficial effects on the host by regulating gastrointestinal (GI) microbiota and protecting against some allergic and autoimmune disorders and inflammatory bowel disease. The potential protective role against inflammatory bowel disease may be related to both modulation of the gut microbiota and the immunomodulatory properties of H. pylori . The inverse association between H. pylori and some potentially proinflammatory and/or procarcinogenic bacteria may suggest it regulates the GI microbiota. Eradication of H. pylori can cause various adverse effects and alter the GI microbiota, leading to short-term or long-term dysbiosis. Overall, studies have shown that gastric Actinobacteria decrease after H. pylori 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 follow-up. Various gastric mucosal bacteria ( Actinomyces , Granulicatella , Parvimonas , Peptostreptococcus , Prevotella , Rothia , Streptococcus, Rhodococcus , and Lactobacillus ) may contribute to precancerous gastric lesions and cancer itself after H. pylori eradication. H. pylori eradication can also lead to dysbiosis of the gut microbiota, with increased Proteobacteria and decreased Bacteroidetes and Actinobacteria. The increase in gut Proteobacteria may contribute to adverse effects during and after eradication. The decrease in Actinobacteria, which are pivotal in the maintenance of gut homeostasis, can persist for &gt; 6 mo after H. pylori eradication. Furthermore, H. pylori eradication can alter the metabolism of gastric and intestinal bacteria. Given the available data, eradication cannot be an unconditional recommendation in every case of H. pylori infection, and the decision to eradicate H. pylori should be based on an assessment of the benefit-risk ratio for the individual patient. Thus, the current guidelines based on the unconditional "test-and-treat" strategy should be revised. The most cautious and careful approach should be taken in elderly patients with multiple eradication failures since repeated eradication can cause antibiotic-associated diarrhea, including severe Clostridioides difficile -associated diarrhea and colitis and antibiotic-associated hemorrhagic colitis due to Klebsiella oxytoca . Furthermore, since eradication therapy with antibiotics and proton pump inhibitors can lead to serious adverse effects and/or dysbiosis of the GI microbiota, supplementation of probiotics, prebiotics, and microbial metabolites ( e.g., butyrate + inulin) should be considered to decrease the negative effects of eradication.

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