H. pylori slyD, a novel virulence factor, is associated with Wnt pathway protein expression during gastric disease
Aining Chu1, Xiuwen Yu1, Qianqian Guo1
1Tumor Etiology and Screening Department of Cancer Institute and General Surgery, The First Hospital of China Medical University, Shenyang, 110001, China; Key Laboratory of Cancer Etiology and Prevention in Liaoning Education Department, The First Hospital of China Medical University, Shenyang, 110001, China; Key Laboratory of GI Cancer Etiology and Prevention in Liaoning Province, The First Hospital of China Medical University, Shenyang, 110001, China.
Abstract:
We have previously reported that the virulence factor HpslyD is related to the occurrence of gastric diseases. However, its mechanism of pathogenesis is still unclear. It is commonly believed that the Wnt/β-catenin pathway is indispensable for the development of gastric cancer, but it is unclear whether HpslyD and Wnt/β-catenin interact during the development of gastric diseases. Therefore, we measured the expression of E-cadherin, β-catenin, TCF4, and CDX2 proteins by IHC in gastric mucosa specimens from patients with different gastric diseases and compared the differences in protein expression to H. pylori-infection status. The results indicated that the expression of these proteins was associated with HpslyD infection. HpslyD subtype infection, rather than common H. pylori infection, may have a greater effect on the expression of Wnt proteins in atrophic gastritis and gastric cancer. Additionally, HpslyD strain infection promoted the expression of Wnt pathway-related proteins with the progression of gastric disease. This study provides insight into the pathogenesis of H. pylori-related gastric diseases and "type-based treatment" for H. pylori infection.
More Related Videos
Related Concept Videos
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
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...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
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.
Peptic Ulcer Disease II: Pathophysiology
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.
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
Gastritis-II: Pathophysiology
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...
Peptic Ulcer Disease I: Introduction
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...


