Scholarlink

Introduction <p><i>Helicobacter pylori</i> is a slow-growing, gram-negative strictly pathogenic bacterium, which colonizes the stomachs of half the global population and is responsible for gastritis, peptic ulcer and even adenocarcinoma, Treatment of choice for eradication is a combination of PPIs and multiple antibiotic therapy. Recently, therapeutic failures began to be attributable to increased antibiotic resistance due to mutations in identified genes <i>(rpoB</i>, 16S rRNA coding gene, <i>gyrA</i>, 23S rRNA coding gene, <i>pbp1A</i>,<i> frxA</i>,<i> rdxA)</i>.</p> Objectives <p>This study aimed to determine, using ultra-deep sequencing, the distribution of mutations in patient s hospitalized or undergoing screening for <i>H. pylori</i>.</p> Methods <p>Gastric biopsies were obtained from two different anatomical regions (antrum/fundus) in 18 patients’ samples from 1998 to 2021, in four French hospitals. Following automated extraction, DNA of <i>H. pylori</i> was amplified using multiplexed PCR, before sequencing on the Illumina iSeq100 platform.</p> Results <p>Antral diversification of <i>H. pylori</i> populations is significantly greater than that at the fundic level for <i>rpoB</i> and <i>rdxA</i>. Fundic diversification of <i>H. pylori</i> populations is significantly greater than that at the antral level for the 23S rRNA coding, <i>rdxA</i> and <i>rpoB</i> genes (<i>p</i> &lt; 0.05), with inter-individual variation.Conversely, the 16S rRNA, frxA, <i>gyrA</i> and pbp1A genes exhibited no significant variation (<i>p</i> &gt; 0.05).</p> Discussion <p>This first study using in-house high-throughput sequencing of <i>H. pylori</i> on clinical biopsies from the same patients reinforces the hypothesis that the bacterial population within the same host is heterogeneous. The presence of minority variants justifies the need for at least two biopsies to ensure robust testing of the <i>H. pylori</i> antibiotic susceptibility profile.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Characterization using ultra-deep sequencing of the intra-host distribution of the mutations associated with H. pylori antibiotic resistance

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月22日

查看全文
  • Laura Chaufour,
  • Alexandra Herve,
  • Birama Ndiaye,
  • Lucie Karayan-Tapon,
  • Médéric Briand,
  • Frédérique Lartigue,
  • Christophe Burucoa,
  • Maxime Pichon

摘要

Introduction

Helicobacter pylori is a slow-growing, gram-negative strictly pathogenic bacterium, which colonizes the stomachs of half the global population and is responsible for gastritis, peptic ulcer and even adenocarcinoma, Treatment of choice for eradication is a combination of PPIs and multiple antibiotic therapy. Recently, therapeutic failures began to be attributable to increased antibiotic resistance due to mutations in identified genes (rpoB, 16S rRNA coding gene, gyrA, 23S rRNA coding gene, pbp1A, frxA, rdxA).

Objectives

This study aimed to determine, using ultra-deep sequencing, the distribution of mutations in patient s hospitalized or undergoing screening for H. pylori.

Methods

Gastric biopsies were obtained from two different anatomical regions (antrum/fundus) in 18 patients’ samples from 1998 to 2021, in four French hospitals. Following automated extraction, DNA of H. pylori was amplified using multiplexed PCR, before sequencing on the Illumina iSeq100 platform.

Results

Antral diversification of H. pylori populations is significantly greater than that at the fundic level for rpoB and rdxA. Fundic diversification of H. pylori populations is significantly greater than that at the antral level for the 23S rRNA coding, rdxA and rpoB genes (p < 0.05), with inter-individual variation.Conversely, the 16S rRNA, frxA, gyrA and pbp1A genes exhibited no significant variation (p > 0.05).

Discussion

This first study using in-house high-throughput sequencing of H. pylori on clinical biopsies from the same patients reinforces the hypothesis that the bacterial population within the same host is heterogeneous. The presence of minority variants justifies the need for at least two biopsies to ensure robust testing of the H. pylori antibiotic susceptibility profile.