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Antigenic mimicry between Helicobacter pylori and gastric mucosa: failure to implicate heat-shock protein Hsp60 using
D E Taylor1, R N Fedorak, R Sherburne
1Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Canada. Diane.Taylor@ualberta.ca
Background:
Helicobacter pylori infection induces autoantibodies that cross-react with human gastric mucosa from infected individuals. Candidates for the antigens responsible for molecular mimicry causing autoreactivity include the heat-shock protein HspB (Hsp60, sometimes called Hsp54) or Lewis x and Lewis y carbohydrate antigens.
Objective:
Our goal was to investigate the involvement of HspB (Hsp60) in autoreactivity between H. pylori and gastric biopsy tissue.
Materials And Methods:
Immunoelectron microscopy was used to study cross-reactivity among biopsy tissues from a patient with gastritis, gastric ulcer, and duodenal ulcer and his own serum as well as reactivity with serum raised against HspB from H. pylori and monoclonal antibodies against Lewis antigens.
Results:
The patient serum reacted with gastric mucosa, and the antibodies involved were predominantly IgG. Antibody raised to H. pylori HspB (Hsp60) reacted only with H. pylori cells but not with gastric mucosal tissue. In contrast, monoclonal antibodies specific for Lewis x and Lewis y antigens reacted with both H. pylori and human gastric epithelial tissue.
Conclusions:
Hsp60 (Hsp54) is unlikely to be involved in autoreactivity seen in individuals infected with H. pylori. In contrast, we could not rule out the role of Lewis x and Lewis y carbohydrate antigens, expressed as a component of H. pylori lipopolysaccharides, in molecular mimicry and autoantibody production.
Insights
Helicobacter pylori infection may trigger autoimmune responses. Heat-shock protein 60 (Hsp60) is unlikely involved, but Lewis x and y antigens might play a role in molecular mimicry and autoantibody production.
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Helicobacter pylori infection can lead to autoantibodies targeting gastric mucosa.
- Potential antigens include heat-shock protein B (HspB/Hsp60) and Lewis antigens (Lewis x, Lewis y).
Purpose of the Study:
- To investigate the role of HspB (Hsp60) in H. pylori-induced autoreactivity against gastric tissue.
Main Methods:
- Immunoelectron microscopy was employed.
- Cross-reactivity was assessed using patient serum, H. pylori HspB-specific antibodies, and anti-Lewis antigen monoclonal antibodies against gastric biopsy tissues.
Main Results:
- Patient serum showed reactivity with gastric mucosa.
- H. pylori HspB antibodies did not react with gastric tissue.
- Lewis x and Lewis y antibodies reacted with both H. pylori and gastric epithelial tissue.
Conclusions:
- Hsp60 (Hsp54) is unlikely to be involved in H. pylori-related autoreactivity.
- Lewis x and Lewis y antigens are potential contributors to molecular mimicry and autoantibody production in H. pylori infection.