Related Experiment Video
Updated: Jun 4, 2026

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes
Published on: July 5, 2024
Induction of a Th17 cell response by Helicobacter pylori Urease subunit B
Jin-Yu Zhang1, Tao Liu, Hong Guo
1Department of Clinical Microbiology and Immunology, College of Medical Laboratory, The Third Military Medical University, Chongqing, PR China.
Abstract:
Th17 cells represent a novel subset of CD4(+) T cells, which is associated with Helicobacter pylori infection. In the present study, we investigated the potential role of Urease subunit B (UreB) in the induction of Th17 cell response. Co-cultured splenic lymphocytes from H. pylori-infected mice with the recombinant UreB (rUreB) elevated IL-17 secretion and caused an increase in the number of Th17 cells. The expression of IL-6 and IL-23 p19 was significantly increased in rUreB-stimulated macrophages. Whole cell protein (WCP) of UreB-deficient strain (UreB(-) strain) induced less Th17 cell responses than that of wild-type strain. In addition, subcutaneous and intranasal immunization of rUreB elicited antigen-specific Th17 cell responses. Intranasal immunization of rUreB reduced H. pylori colonization in the stomach, which was closely related with the increased rUreB-specific Th17 cell responses. These results suggest that UreB is an important protein which is able to elicit Th17 cell responses against H. pylori both in vivo and in vitro.
More Related Videos
10:44One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
Published on: June 18, 2016
09:05High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability
Published on: November 21, 2014
Related Concept Videos
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
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
Peptic Ulcer
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 to M3...