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pubmed-article:21637017pubmed:dateCreated2011-6-3lld:pubmed
pubmed-article:21637017pubmed:abstractTextHelicobacter pylori is the primary cause of peptic ulcer disease and is estimated to account for about 60% of all cases of gastric cancer, the second most common cause of cancer death worldwide. Among the H. pylori virulence factors associated with disease, in addition to the well-known cag pathogenicity island, is the BabA adhesin, an outer membrane protein that binds with high affinity to fucosylated glycans on the gastric epithelium, such as Lewis B (Le(b)) and related terminal fucose residues found on the blood group O (H antigen), A and B antigens. BabA-mediated attachment to the gastric mucosa promotes chronic inflammation and gastric pathology, which from the bacterial perspective carries both risks and benefits. We recently described modulation in expression of BabA and related outer membrane proteins that occurs during colonization of experimental animals. Here we put these findings into a broader context, and speculate on their implications for the host-pathogen relationship.lld:pubmed
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pubmed-article:21637017pubmed:authorpubmed-author:SolnickJay...lld:pubmed
pubmed-article:21637017pubmed:authorpubmed-author:MooreMary EMElld:pubmed
pubmed-article:21637017pubmed:authorpubmed-author:BorénThomasTlld:pubmed
pubmed-article:21637017pubmed:copyrightInfo© 2011 Landes Biosciencelld:pubmed
pubmed-article:21637017pubmed:issnTypeElectroniclld:pubmed
pubmed-article:21637017pubmed:volume2lld:pubmed
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pubmed-article:21637017pubmed:articleTitleLife at the margins: modulation of attachment proteins in Helicobacter pylori.lld:pubmed
pubmed-article:21637017pubmed:affiliationDepartment of Medicine, Center for Comparative Medicine, California National Primate Research Center, University of California, Davis School of Medicine, Davis, CA 95616, USA.lld:pubmed
pubmed-article:21637017pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21637017pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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