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Molecular mimicry between Helicobacter pylori and the host
B J Appelmelk1, R Negrini, A P Moran
1Dept of Medical Microbiology, Vrije Universiteit, Amsterdam, The Netherlands. bj.appelmelk.mm@med.vu.nl
Trends in Microbiology
|February 1, 1997
Summary
Helicobacter pylori infection triggers an autoimmune response. Antibodies against bacterial lipopolysaccharide (LPS) mistakenly target gastric cells expressing similar antigens, causing inflammation.
Area of Science:
- Microbiology
- Immunology
- Gastroenterology
Background:
- Helicobacter pylori infection is a major cause of gastritis and peptic ulcers.
- The bacterium's lipopolysaccharide (LPS) shares structural similarities with host Lewis antigens in the gastric mucosa.
- This molecular mimicry may play a role in the host's immune response during infection.
Purpose of the Study:
- To investigate the role of Helicobacter pylori LPS in inducing autoimmune responses against the gastric mucosa.
- To determine if antibodies generated against H. pylori LPS can cross-react with host Lewis antigens.
Main Methods:
- Analysis of H. pylori LPS for Lewis x and Lewis y antigen expression.
- Serological studies to detect antibodies against H. pylori LPS in infected individuals.
- Immunohistochemical analysis of gastric biopsies to assess antibody binding to host tissues.
Main Results:
- Helicobacter pylori LPS was confirmed to express Lewis x and Lewis y blood group antigens.
- Antibodies against H. pylori LPS were found to bind to Lewis antigens on gastric glycoproteins.
- This cross-reactivity suggests a mechanism for autoimmune inflammation in H. pylori-infected individuals.
Conclusions:
- The expression of Lewis antigens by H. pylori LPS is a key factor in initiating autoimmune responses.
- Antibodies targeting H. pylori LPS can lead to autoimmune gastritis through molecular mimicry.
- Understanding this mechanism could lead to new therapeutic strategies for H. pylori-associated gastric diseases.