慢性吸烟暴露掩盖了Helicobacter pylori感染的病理特征,同时促进了瘤发作
Maeve T Morris1, Benjamin C Duncan1, M Blanca Piazuelo2
1Department of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, West Virginia.
Cancer prevention research (Philadelphia, Pa.)
|January 10, 2025
概括
香烟烟雾可能会隐藏Helicobacter pylori感染症状,但通过增加DNA损伤来加速胃癌. 吸烟者有H. pylori需要查,以降低癌症风险.
科学领域:
- 胃肠病学 胃肠病学
- 在瘤学瘤学.
- 微生物学 微生物学
背景情况:
- 胃癌是全世界主要的死亡原因之一.
- 杆菌感染和吸烟是主要的危险因素.
- 在胃癌的发展中,H. pylori和香烟烟雾 (CS) 之间的相互作用尚未完全理解.
研究的目的:
- 调查香烟烟雾对H. pylori病原和胃癌发病的直接影响.
主要方法:
- 雄性C57BL/6小鼠感染了H. pylori,并暴露在CS或过空气 (FA) 中8周.
- 评估了胃形态,炎症,DNA损伤和癌前病变.
主要成果:
- 在模拟感染小鼠中,CS暴露并没有改变粗胃形态或炎症.
- CS显著减轻了H. pylori引起的胃炎症,缩和转化等.
- 尽管炎症减少了,但CS增加了DNA损伤,并在感染H. pylori的小鼠中加速了发育不良.
结论:
- 吸烟可能会掩盖H. pylori感染的病理症状,同时促进DNA损伤和加速胃癌发生.
- 被H. pylori感染的吸烟者可能会有沉默的疾病表现,但患胃癌的风险增加.
- 对感染H. pylori的吸烟者进行查对于预防胃癌至关重要.
相关概念视频
Peptic Ulcer Disease I: Introduction
131
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...
131
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
325
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...
325
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
537
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...
537
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
353
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.
353
Gastritis-II: Pathophysiology
233
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...
233
Peptic Ulcer Disease II: Pathophysiology
267
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.
267


