Related Experiment Video
Updated: May 5, 2026

Hot Biological Catalysis: Isothermal Titration Calorimetry to Characterize Enzymatic Reactions
Published on: April 4, 2014
Influence of pH on metabolism and urease activity of Helicobacter pylori
M Rektorschek1, D Weeks, G Sachs
1Department of Molecular Biology, Byk Gulden Pharmaceuticals, Konstanz, Germany.
Background & Aims:
The metabolic and urease responses of Helicobacter pylori to variations in gastric acidity are unknown. The aim of this study was to determine effects of changes of environmental pH on metabolism, urease activity, and survival of H. pylori in an unbuffered environment.
Methods:
Bacterial metabolism and urease activity were determined by measuring pH changes in perfused microphysiometer chambers over a pH range from 2.5 to 9.0 with or without urea and survival by restoration of metabolism at pH 7.4.
Results:
Glucose metabolism by acid-adapted H. pylori occurred at a perfusion pH between 3.5 and 8.6 and was highest between 7.4 and 8.2. Metabolism was irreversibly inhibited at pH <3.5 or >8.6. In the presence of 2.5 mmol/L urea, the chamber pH increased to about 6.2 during perfusion between pH 5.5 and 4.0. At pH 4.0 and below, urease activity increased several-fold without change of chamber pH. Urea in the perfusate enabled retention of metabolism after acid exposure but was toxic at pH 7.4.
Conclusions:
The metabolic range of acid-adapted H. pylori is between an environmental pH of 3.5 and 8.6. Extracellular pH-regulated internal urease activity allows metabolism in the pH range between 4.0 and 2. 5 by maintaining periplasmic pH at 6.2. The organism is an acid-tolerant neutralophile due to internal urease activity.
More Related Videos
05:23Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 2025
04:56Detection of Helicobacter pylori Infection and Antibiotic Resistance via Stool Quantitative Polymerase Chain Reaction Analysis
Published on: May 16, 2025
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...
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
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.
Factors Influencing Microbial Growth: pH
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology