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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
Abstract:
Helicobacter pylori lipopolysaccharide (LPS) expresses Lewis x and Lewis y blood group antigens that are identical to those occurring in the human gastric mucosa. During infection, antibodies against LPS, which bind to host Lewis antigens, may be induced. These consequently recognize gastric glycoprotein targets and cause autoimmune inflammation.
Insights
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.