Clarithromycin increases the release of heat shock protein B from Helicobacter pylori
1First Department of Internal Medicine, Nagoya University School of Medicine, Showa-ku, Nagoya, Japan.
Background:
Clarithromycin (CAM) may have certain indirect effects on Helicobacter pylori (H. pylori) other than its inhibitory activity on bacterial growth, as indicated in other infections with Gram-negative micro-organisms. In the present study, we examined the effects of lower concentrations of CAM on the release of heat shock protein B (HspB), one of the major antigenic proteins from H. pylori cells, as well as the changes in humoral immune response and histological degree of antral gastritis in patients who received eradication therapy with CAM.
Methods:
The H. pylori strain 26695 and three CAM-resistant clinical isolates were cultured in broth with and without CAM (2-500 ng/mL). Expression of H. pylori proteins was examined by two-dimensional (2D)-electrophoresis followed by N-terminal amino acid sequencing. Changes in host immune response and histological degree of antral gastritis were monitored in patients with peptic ulcer disease who received H. pylori eradication therapy.
Results:
2D electrophoresis showed 26 spots in extracellularly released proteins with different profiles from those in cytoplasmic proteins. The release of HspB increased after incubation with CAM (30-500 ng/mL) in all three H. pylori clinical isolates tested. Patients with failed H. pylori eradication after triple therapy with CAM, but not those with failed eradication after dual therapy without CAM, showed an increase in serum IgG1 and IgG2 antibodies against HspB along with a decrease in the degree of neutrophil and H. pylori colonization density in tissue sections.
Conclusions:
CAM may induce a humoral immune response against H. pylori and a decrease in gastric mucosal inflammation through up-regulation of the release of HspB from the bacteria in infected patients.
Insights
Clarithromycin (CAM) may enhance the release of heat shock protein B (HspB) from Helicobacter pylori (H. pylori). This may boost the immune response against H. pylori and reduce gastric inflammation in patients.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Clarithromycin (CAM) may exert indirect effects on Helicobacter pylori (H. pylori) beyond growth inhibition.
- Investigating lower CAM concentrations on H. pylori heat shock protein B (HspB) release and host immune response is crucial.
Purpose of the Study:
- To examine the effects of sub-inhibitory concentrations of CAM on HspB release from H. pylori.
- To assess changes in humoral immune response and gastric inflammation in patients undergoing H. pylori eradication therapy with CAM.
Main Methods:
- H. pylori strains were cultured with varying CAM concentrations (2-500 ng/mL).
- Protein expression was analyzed using 2D-electrophoresis and N-terminal sequencing.
- Host immune response and histological gastritis were monitored in patients receiving H. pylori eradication therapy.
Main Results:
- CAM (30-500 ng/mL) increased HspB release in all tested H. pylori clinical isolates.
- Patients with failed CAM-based triple therapy showed increased anti-HspB IgG1/IgG2 antibodies.
- These patients also exhibited reduced neutrophil infiltration and H. pylori colonization.
Conclusions:
- CAM may induce a humoral immune response against H. pylori.
- CAM might decrease gastric mucosal inflammation by up-regulating HspB release from H. pylori.
More Related Videos
06:40Quantitative Polymerase Chain Reaction (qPCR)-Based Rapid Diagnosis of Helicobacter pylori Infection and Antibiotic Resistance
Published on: July 28, 2023
05:23Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
Published on: March 7, 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 to M3...
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
Other Stress Responses in Bacteria
Diversity of Archaea III
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
