Binding of Helocobacter pyori to Human Gastric Mucose: Identification and Characterization of a Lewis b Bingind Protein.
Abstract
For nearly fifty years, it has been well known by epidemiologists that individuals expressing the 0 blood group phenotype have a higher risk of developing gastric and duodenal ulcers than individuals with A or B blood group phenotypes. Because the etiology of the disease was not understood, this phenomenon remained a mystery for decades. With the isolation of a Gram-negative, spiral shaped bacterium from human gastric mucosa, Helicobacter pylori, came the answers to many questions concerning peptic ulcer disease, including this one. Recently,.it has been shown that the Lewis (Leb) blood group antigen, expressed both on blood cells and gastric epithelium, acts as a specific receptor for H. pylori. Leb is the major blood group antigen in the Lewis system expressed in individuals with the 0 phenotype. In individuals of the A or B blood group phenotype, this epitope is usually modified with either a terminal GalNaca1.3 or Gala1.3, respectively. The lectin-like specificity of the host cell:bacterial cell interaction strongly implies that a Leb specific adhesin is present on the surface of the microorganism. We aim to identify and characterize this adhesin not only to gain valuable knowledge of the pathogenesis of H. pylori, but because of its role as a potential vaccine candidate. In the course of this three year study, we plan to purify the Leb specific adhesin, clone and mutagenize the gene encoding it, and assess its priority as a possible vaccine candidate. We also plan to evaluate transgenic mice for their use as an animal model for Le sub b dependent colonization of gastric epithelia.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 1995
- Accession Number
- ADA344185
Entities
People
- Susan D. Biegel
Organizations
- University of North Carolina at Chapel Hill