Why Helicobacter pylori has Lewis antigens
ABSTRACT In mimicry with human gastric epithelial cells, the lipopolysaccharide of Helicobacter pylori expresses Lewis blood group antigens. Recent data suggest that molecular mimicry does not promote immune evasion, nor does it lead to induction of autoantibodies, but that H. pylori Lewis X mediates adhesion to gastric epithelial cells and is essential for colonization.
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ABSTRACT: We compared the serological reactivity of lipopolysaccharides (LPS) isolated from Japanese and Western strains of Helicobacter pylori against anti-Lewis antigen monoclonal antibodies and H. pylori-positive Japanese sera. The two LPS from Western strains (26695 and O:2) did not react with any sera from Japanese patients, while all LPS from Japanese strains and the Sydney strain reacted with these sera. We propose that LPS of all Japanese smooth strains share either one of two epitopes, which are termed highly antigenic and weakly antigenic epitopes, present in the O-polysaccharide portion, and these epitopes are independent the Lewis antigens. The present findings indicated that the two Western strains lacked the two epitopes, which are shared by all Japanese strains.ISRN microbiology. 01/2012; 2012:162816.
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ABSTRACT: Helicobacter pylori is an adapted gastric pathogen that colonizes the human stomach, causing severe gastritis and gastric cancer. A hallmark of infection is the ability of this organism to evade detection by the human immune system. H. pylori has evolved a number of features to achieve this, many of which involve glyco-conjugates including the lipopolysaccharide, peptidoglycan layer, glycoproteins, and glucosylated cholesterol. These major bacterial components possess unique features from those of other gram-negative organisms, including differences in structure, assembly, and modification. These defining characteristics of H. pylori glycobiology help the pathogen establish a long-lived infection by providing camouflage, modulating the host immune response, and promoting virulence mechanisms. In this way, glyco-conjugates are essential for H. pylori pathogenicity and survival, allowing it to carve out a niche in the formidable environment of the human stomach.Gut Microbes 07/2013; 4(6).
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ABSTRACT: Crohn's disease and ulcerative colitis are chronic dis- abling inflammatory bowel diseases (IBDs). Although the causes of IBD are unknown, defects in innate and adaptive immune pathways have been identified and biological therapies that target key molecules have been designed. Infliximab, a chimeric immunoglobulin (Ig)G1 monoclonal antibody to tumor necrosis factor, dramatically improved treatment of patients with Crohn's disease and ulcerative colitis. Infliximab has achieved treatment goals such as mucosal healing and decreasing the need for hospitalizations and surgeries. Although several anti-tumor necrosis factor therapies have been developed, there is a great need for drugs that target other pathways. Natalizumab, an antibody against the integrin 4 subunit, blocks leukocyte adhe- sion and has reached the clinic in the United States but has not been approved in the European Union; other anti-adhesion molecules currently are under develop- ment. Additional approaches under clinical develop- ment include therapeutics that target cytokines, such as interleukin-12/23, as well as those that block T-cell sig- naling. The use of recombinant human proteins, in- cluding immunoregulatory cytokines and growth fac- tors, has not been successful so far. The efficacy of each therapy must be shown in carefully designed clinical programs. Biological therapies carry a definite safety risk, so their place in treatment algorithms must be defined carefully.