在肝硬化患者的肠道微生物群和骨髓硬化相关性研究
Ninghui Zhao1, Jinjia Bai1, Xinmiao Li1
1Department of Gastroenterology, Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, China.
Frontiers in nutrition
|February 19, 2025
概括
肠道微生物群的组成在肝硬化患者和肌骨瘤患者中不同. 像Roseburia hominis这样的特定细菌可以作为诊断肝硬化患者肌骨瘤的非侵入性生物标志物.
科学领域:
- 胃肠病学 胃肠病学
- 微生物学 微生物学
- 生物标志物发现发现
背景情况:
- 肝硬化与肌肉骨病有关,肌肉脂肪透的特征.
- 肠道微生物群在肝硬化中肌肉骨病的发展中的作用尚不清楚.
研究的目的:
- 为了研究肠道微生物群的特征,在肝硬化患者与骨髓炎.
- 为了确定特定的细菌物种,涉及到骨髓病变的发病.
- 评估肠道微生物群对肌肉骨病的诊断潜力.
主要方法:
- 使用元基因组测序 (metagenomic sequencing) 对 (n=44) 和没有 (n=36) 骨髓炎的肝硬化患者的肠道微生物组组成进行比较.
- 分析了细菌物种丰富度与肌肉衰减密度之间的关联.
- 通过使用ROC曲线评估已识别的细菌对肌骨瘤的诊断价值.
主要成果:
- 在两组之间观察到15种细菌物种相对丰度的显著差异.
- 罗兹布里亚Hominis和Subdoligranulum未分类显示与肌肉脂肪的反向关联.
- 罗斯布里亚人类 (AUC=0.869) 和未分类的Subdoligranulum (AUC=0.828) 显示了肌肉骨病的诊断潜力.
结论:
- 肠道微生物群的组成在患有肌肉骨病的肝硬化患者中发生了变化.
- 罗兹布里亚人类和未分类的Subdoligranulum可能作为肌肉骨病的非侵入性生物标志物.
- 准肠道微生物群可能为肝硬化中的骨髓炎提供新的治疗策略.
相关概念视频
01:17Gastritis-II: Pathophysiology
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
01:27Microbiota of the Stomach and Small Intestine
The human gastrointestinal (GI) tract is characterized by distinct physicochemical conditions that shape its microbial communities. Among these, the stomach presents a particularly challenging environment for microbial colonization due to its highly acidic pH, ranging from 1 to 3. This extreme acidity effectively limits microbial density. However, certain acid-tolerant microorganisms are capable of surviving in this niche. Notably, Helicobacter pylori can colonize the gastric mucosa,...
01:18Dysbiosis of the Gut Microbiota
The human gut microbiome includes a diverse array of microbial species, including beneficial commensals and opportunistic pathogens, which interact to support host health. These microbes contribute to essential functions such as nutrient metabolism, immune system modulation, and maintenance of intestinal barrier integrity. However, disruptions to this equilibrium—referred to as dysbiosis—can have widespread physiological consequences.Dysbiosis is often characterized by reduced microbial...
01:26Gastritis II: Pathophysiology
The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
01:23Cirrhosis I: Introduction
Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
01:24Cirrhosis II: Pathophysiology
Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...