Refractory Helicobacter pylori infection and the gastric microbiota.
Refractory Helicobacter pylori infection and the gastric microbiota.
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难治性幽门螺杆菌感染与胃微生物群
DOI：
10.3389/fcimb.2022.976710
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发表时间：
2022
影响因子：
5.7
通讯作者：
中科院分区：
文献类型：
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作者：
治疗难治性幽门螺杆菌感染是困难的。此外，目前还没有关于难治性幽门螺杆菌感染的胃微生物群的研究。我们设计了一项临床回顾性研究，涉及32名受试者，分为三组：1。nAGHp。a、treatment-naïve幽门螺旋杆菌感染患者；2. nAGHp。b，幽门螺杆菌阴性患者；和3。EFHp。a，难治性幽门螺杆菌感染患者。收集本研究中心生物库胃粘膜样本进行16S rRNA测序分析，并通过PICRUSt预测细菌功能。幽门螺杆菌阳性组与幽门螺杆菌阴性组在物种多样性、胃微生物群结构、细菌功能等方面存在显著差异。与难治性幽门螺杆菌感染组相比，幽门螺杆菌阳性组有益乳杆菌显著富集。细菌相互作用网络图显示，难愈幽门螺杆菌感染组菌群相互作用减少。难愈性幽门螺旋杆菌感染组胃微生物群富集于代谢和传染病途径(能量代谢、细菌分泌系统、谷胱甘肽代谢、蛋白质折叠及相关加工、硫代谢、膜和细胞内结构分子、脂多糖生物合成、泛醌等萜类醌生物合成、无机离子转运和代谢；以及辅助因子和维生素的代谢)，与未经治疗的幽门螺杆菌阳性组相比。当多次根除幽门螺杆菌失败时，胃微生物群发生显著变化。多次幽门螺杆菌感染的根除史在一定程度上导致胃黏膜菌群失衡，主要表现为抑制胃内有益乳杆菌的生长。难治性幽门螺杆菌感染患者发生胃癌的风险可能高于其他幽门螺杆菌阳性患者。
Curing refractory Helicobacter pylori infection is difficult. In addition, there is currently no research on the gastric microbiota of refractory H. pylori infection. We designed a clinical retrospective study involving 32 subjects divided into three groups: 1. nAGHp.a, treatment-naïve patients with H. pylori infection; 2. nAGHp.b, H. pylori-negative patients; and 3. EFHp.a, patients with refractory H. pylori infection. Gastric mucosal samples from the biobank of our research center were collected for 16S rRNA sequencing analysis and bacterial functions were predicted via PICRUSt. There were significant differences between the H. pylori- positive group and the H. pylori-negative group in species diversity, gastric microbiota structure, and bacterial function. The beneficial Lactobacillus in the H. pylori-positive group were significantly enriched compared with those in the refractory H. pylori infection group. The bacterial interaction network diagram suggested that the microbiota interactions in the refractory H. pylori infection group decreased. The gastric microbiota of the refractory H. pylori infection group was enriched in the pathways of metabolism and infectious diseases (energy metabolism, bacterial secretion system, glutathione metabolism, protein folding and associated processing, sulphur metabolism, membrane and intracellular structural molecules, lipopolysaccharide biosynthesis, ubiquinone and other terpenoid-quinone biosynthesis, inorganic ion transport and metabolism, and metabolism of cofactors and vitamins) when compared with the H. pylori-positive group without treatment based on PICRUSt analysis. Significant alterations occurred in the gastric microbiota when eradication of H. pylori failed multiple times. A history of eradication of multiple H. pylori infections leads to an imbalance in the gastric mucosal microbiota to a certain extent, which was mainly reflected in the inhibition of the growth of beneficial Lactobacillus in the stomach. Patients with refractory H. pylori infection may be at a higher risk of developing gastric cancer than other H. pylori-positive patients.