在非性消化不良和胃患者中比较胃微生物群概况
Silva Polat Sari1, Aliye Soylu2, Kivanc Derya Peker3
1Vocational School of Health Services, Istanbul Aydin University, Istanbul, 34295, Turkey.
BMC microbiology
|December 15, 2025
概括
在胃肠道疾病中缺乏Helicobacter pylori (H. pylori) 与口腔细菌如Alloprevotella,Porphyromonas和Neisseria的增加有关. 这项研究为土耳其患者的胃微生物生态提供了新的见解.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 人类健康 人类健康 人类健康
背景情况:
- 人的胃内有着多样化的微生物群,不仅仅是Helicobacter pylori (H. pylori).
- 当H. pylori缺席时,口腔细菌可能会主导胃,但它们在胃肠疾病中的作用尚不清楚.
- 了解胃微生物的变化对于诊断和治疗胃疾病至关重要.
研究的目的:
- 分析和比较土耳其患者的胃微生物组合,非性消化不良 (NUD) 和胃病 (PUD).
- 调查这些患者群体中H. pylori状态和胃微生物特征之间的关联.
- 阐明口腔来源细菌在H. pylori阴性胃肠疾病中的作用.
主要方法:
- 98名患者进行了内镜评估,并分为NUD (n=52) 和PUD (n=46) 组.
- 胃活检样本使用定量实时PCR (qPCR) 分析了H. pylori的相对丰度.
- 下一代测序被用于全面的胃微生物群概况.
主要成果:
- 在71.4%的样本中检测到H. pylori DNA,PUD (82.6%) 的患病率高于NUD (61.5%) 的患者 (p=0.02).
- 阴性H. pylori的NUD患者表现出更高的Alloprevotella丰度 (p<0.05).
- 与H. pylori阴性NUD患者相比,H. pylori阴性PUD患者的Porphyromonas和Neisseria增加 (p<0.05),这表明口腔细菌的机会性扩张.
结论:
- 在胃部疾病中缺少H. pylori与微生物群组成的显著转变有关.
- 口腔来源的细菌 (Alloprevotella,Porphyromonas,Neisseria) 增加了H. pylori阴性胃肠疾病的发生.
- 这项研究为NUD和PUD的土耳其患者的胃微生物生态提供了新的区域洞察力.
相关概念视频
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
507
Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
507
Peptic Ulcer Disease I: Introduction
711
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
711
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
1.1K
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
1.1K
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
1.1K
Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
1.1K
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
1.1K
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
1.1K
Peptic Ulcer Disease II: Pathophysiology
1.9K
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
1.9K


