H. pylori eradication with antibiotic treatment causes changes in glucose homeostasis related to modifications in the gut microbiota

PLoS One. 2019 Mar 14;14(3):e0213548. doi: 10.1371/journal.pone.0213548. eCollection 2019.

Abstract

Background: H. pylori infection and eradication cause perturbations of the gut microbiome. The gut microbiota has been identified as a potential contributor to metabolic diseases. We evaluate whether these alterations in intestinal microbiota composition produced by H. pylori infection and its posterior eradication with antibiotic treatment could be associated with glucose homeostasis in metabolically healthy subjects.

Methods: Forty adult patients infected with H. pylori and 20 control subjects were recruited. The infected subjects were evaluated before and two months after eradication treatment (omeprazole, clarithromycin, amoxicillin). The microbiota composition in fecal samples was determined by 16S rRNA gene (V3-V4) sequencing using Illumina Miseq.

Results: Patients (pre- and post-H. pylori eradication) showed a decreased bacterial richness and diversity with respect to controls. There was an improvement in glucose homeostasis in subjects two months after H. pylori eradication treatment. Changes in the amount of Rikenellaceae, Butyricimonas, E. biforme, B. fragilis, and Megamonas were inversely associated with changes in the glucose level or related parameters (Hb1ac) in H. pylori eradication subjects.

Conclusions: H. pylori infection and eradication with antibiotic treatment causes alteration of the human gut microbiome. The increase in SCFA-producing bacteria and glucose-removing bacteria, specifically members of Megamonas, Rikenellaceae and Butyricimonas, has been related with an improvement in glucose homeostasis after H. pylori eradication with antibiotic treatment.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Amoxicillin / administration & dosage*
  • Anti-Bacterial Agents / administration & dosage*
  • Clarithromycin / administration & dosage*
  • Female
  • Gastrointestinal Microbiome / drug effects*
  • Gastrointestinal Microbiome / genetics
  • Glucose / metabolism*
  • Helicobacter Infections / drug therapy*
  • Helicobacter Infections / genetics
  • Helicobacter Infections / metabolism
  • Helicobacter Infections / microbiology
  • Helicobacter pylori / genetics
  • Helicobacter pylori / metabolism*
  • Homeostasis / drug effects*
  • Humans
  • Male
  • Middle Aged
  • Omeprazole / administration & dosage*
  • RNA, Bacterial / genetics
  • RNA, Ribosomal, 16S / genetics
  • Sequence Analysis, RNA

Substances

  • Anti-Bacterial Agents
  • RNA, Bacterial
  • RNA, Ribosomal, 16S
  • Amoxicillin
  • Clarithromycin
  • Glucose
  • Omeprazole

Grants and funding

This work was supported in part by a grant from the Instituto de Salud Carlos III and co-funded by Fondo Europeo de Desarrollo Regional - FEDER, PI14/00082, PI15/01114, Madrid, Spain, and by the “Centros de Investigación Biomédica en Red” (CIBER) of the Institute of Health Carlos III (ISCIII) (CB06/03/0018). I.C.P is the recipient of a postdoctoral grant (Rio Hortega CM17/00169) from the Spanish Ministry of Economy and Competitiveness (Carlos III Institute of Health) and co-funded by Fondo Europeo de Desarrollo Regional - FEDER. I.M.I was supported by a ‘‘Miguel Servet Type I’’ contract from the Instituto de Salud Carlos III (CP16/00163) and co-funded by Fondo Europeo de Desarrollo Regional - FEDER. AMG is the recipient of a postdoctoral grant (Rio Hortega CM14/00078) and is now the recipient of a postdoctoral grant (Juan Rodes CM 17/00023) from the Spanish Ministry of Economy and Competitiveness (Carlos III Institute of Health) and co-funded by Fondo Europeo de Desarrollo Regional - FEDER. FC was supported by a “Nicolas Monarde” contract (C-0032-2016) from Servicio Andaluz de Salud.