超尿血症通过调节肠道微生物群来驱动肠道屏障功能障碍
Xiaomin Yang1, Dan Liu2, Xiangzhong Zhao3
1Laboratory Medicine, the Affiliated Hospital of Qingdao University, Qingdao, 266003, PR China.
Heliyon
|September 3, 2024
概括
肠道微生物群在高尿血症中直接导致肠道屏障功能障碍. 用氨醇和抗生素治疗改善了肠道透性并减少了炎症,但去除微生物使代谢问题恶化.
科学领域:
- 胃肠病学 胃肠病学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 众所周知,高尿路血症会增加肠道的透性.
- 通过高尿素血症损害肠道屏障的具体机制尚不清楚.
研究的目的:
- 调查肠道微生物群在高尿血症引起的肠道屏障功能障碍中的作用.
- 确定关键的分子参与者和治疗点.
主要方法:
- 通过使用腺素和奥特拉西尔,建立了超尿血症的小鼠模型.
- 治疗包括阿洛普里诺尔 (减少尿酸),抗生素 (减少微生物群) 和无菌条件.
- 评估了肠道透性,肠道微生物组成 (16S rRNA测序),炎症标记物 (IL-1β,TNF-α) 和紧结蛋白.
主要成果:
- 阿洛普林醇降低了肠道透性和TNF-α水平.
- 抗生素部分缓解了透性,同时消除了肠道微生物群,加剧了脂质代谢功能障碍.
- 免受肠道损伤保护的无菌小鼠的超尿血,以及调节炎症和紧结基因表达的治疗.
结论:
- 肠道微生物群是高尿血症中肠道屏障功能障碍的直接和特定贡献者.
- 准肠道微生物群和尿酸水平显示出治疗潜力,用于管理与高尿血症相关的肠道问题.
相关概念视频
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
358
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.
358
Irritable Bowel Syndrome I: Introduction
263
Irritable Bowel Syndrome (IBS) is characterized by functional disturbances in the gastrointestinal system, presenting a cluster of symptoms without evident structural or biochemical abnormalities. It primarily affects the large intestine and may cause abdominal pain, bloating, excessive gas, diarrhea, constipation, or both.
IBS is a chronic condition that can persist over a long period or recur frequently.
The pathogenesis of IBS involves a complex interplay of the following factors:
Altered...
IBS is a chronic condition that can persist over a long period or recur frequently.
The pathogenesis of IBS involves a complex interplay of the following factors:
Altered...
263
Peptic Ulcer Disease I: Introduction
148
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...
148
Gastritis-II: Pathophysiology
286
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...
286
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
545
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...
545
Peptic Ulcer Disease II: Pathophysiology
334
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.
334


