杆菌CagA+菌株通过调节肠道菌群来调节结直肠病理
Shasha Cui1, Xinqiang Liu2, Fengxia Han1
1Clinical Laboratory, Binzhou People's Hospital, No.515, Huangheqi Road, Bincheng District, Binzhou, Shandong Province, 256610, P. R. China.
BMC gastroenterology
|February 5, 2025
概括
杆菌 (HP) CagA+菌株诱导肠道微生物群失生,导致肠道屏障受损,并可能通过Staphylococcus和Corynebacterium殖民增加结肠直肠癌风险.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 在瘤学瘤学.
背景情况:
- 杆菌 (HP) 感染是已知的胃疾病的风险因素.
- 惠普的CagA蛋白与病毒毒性增加有关.
- 通过肠道微生物群调节在结直肠病变中HP CagA+菌株的作用仍在研究中.
研究的目的:
- 研究HP CagA+菌株对结直肠病变的影响.
- 探索肠道微生物群失生症在HP CagA+诱导的结直肠变化的作用.
- 评估HP CagA+感染与炎症标志物之间的关联.
主要方法:
- C57BL/6J小鼠感染了HP CagA+菌株,HP CagA-菌株或对照介质.
- 使用Giemsa,H&E染色和16SrRNA测序分析了胃和结肠直肠组织.
- 量化了IL-6,IL-8,IL-10和TNF-α的血清水平.
主要成果:
- 惠普CagA+感染导致结直肠炎症,增加MHC II表达,以及血清炎症细胞因子 (TNF-α,IL-6,IL-8,IL-10) 的升高.
- 观察到肠道微生物群失调,其特点是微生物组分布发生变化,F/B比率降低,以及α多样性降低 (Chao1,Shannon).
- 在对照组和HP CagA+组之间观察到β多样性的显著差异,HP CagA+组的Staphylococcus和Corynebacterium的丰富.
结论:
- 惠普CagA+菌株诱导肠道微生物群失调,导致肠道屏障的破坏.
- 这种失生症可能会影响结肠直肠癌的发展,因为它会促进特定细菌的殖民,比如Staphylococcus和Corynebacterium.
- 惠普CagA+感染引发炎症反应并改变肠道微生物组成,突出显示了与结直肠病理的潜在联系.
相关概念视频
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
527
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...
527
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
347
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.
347
Gastritis-II: Pathophysiology
215
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...
215
Peptic Ulcer Disease I: Introduction
123
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...
123
Bacterial Flora of the Large Intestine
375
The gut microbiome is formed by a vast and diverse community of bacteria that colonizes our large intestine. These bacteria start residing in the gut from birth and continue diversifying throughout life, influenced by factors such as diet, lifestyle, and stress. The gut bacterial community also includes bacteria from food and those that enter the colon through the anus.
The normal gut flora of the colon plays a critical role in generating essential vitamins such as vitamins K, B5, and B7.
The normal gut flora of the colon plays a critical role in generating essential vitamins such as vitamins K, B5, and B7.
375
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
320
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...
320


