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Metastability of Helicobacter pylori bab adhesin genes and dynamics in Lewis b antigen binding
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
Vise andre og tillknytning
2004 (engelsk)Inngår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 101, nr 48, s. 16923-16928Artikkel i tidsskrift (Fagfellevurdert) Published
sted, utgiver, år, opplag, sider
2004. Vol. 101, nr 48, s. 16923-16928
Emneord [en]
Adhesins; Bacterial/*genetics/immunology, Base Sequence, Blotting; Northern, Blotting; Southern, Helicobacter pylori/*genetics, Lewis Blood-Group System/*immunology, Microscopy; Fluorescence, Molecular Sequence Data, RNA; Messenger/genetics, Recombinant Fusion Proteins/immunology
Identifikatorer
URN: urn:nbn:se:umu:diva-6648DOI: 10.1073/pnas.0404817101PubMedID: 15557006OAI: oai:DiVA.org:umu-6648DiVA, id: diva2:146318
Tilgjengelig fra: 2007-12-16 Laget: 2007-12-16 Sist oppdatert: 2018-06-09bibliografisk kontrollert
Inngår i avhandling
1. Helicobacter pylori: molecular mechanisms for variable adherence properties
Åpne denne publikasjonen i ny fane eller vindu >>Helicobacter pylori: molecular mechanisms for variable adherence properties
2009 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

More than half of all people worldwide are infected with H. pylori. The infection always cause a gastric inflammation that may develop into peptic ulcer disease or gastric cancer. Attachment proteins, adhesins, mediate specific adherence of H. pylori to receptor structures on the human gastric mucosa. The best-characterized H. pylori adhesin-receptor interactions are the BabA adhesin and the binding to the fucosylated blood group antigens ABO/Lewis b (Leb) and the SabA adhesin and its binding to the inflammation associated sialyl-Lewis x antigen. During H. pylori infection the availability of receptor structures on the human gastric mucosa changes as a consequence of the host inflammatory and immune responses. Consequently the bacterial population need to adjust its adherence properties to stay colonized. This thesis describes mechanisms that generate H. pylori populations with variable adherence properties and mechanisms for adjustment of adhesin expression levels.In H. pylori strains devoid of Leb-binding, we found bacterial cells with Leb-binding. Isolation of such H. pylori clones demonstrated that the change in receptor binding phenotype was obtained via the mechanisms of homologous recombination and slipped strand mispairing (SSM). Disease presentation in relation to BabA expression was studied in H. pylori infected Mongolian gerbils. We showed that BabA was not essential for colonization but caused severe injury to the gastric mucosa and was turned off during long-term infection by nucleotide changes within the babA gene. Gerbils infected with BabA-weak-expressing strains maintained BabA expressing clones for a longer period than gerbils that were infected with BabA-high-expressing strains. Studies of the gerbil gastric mucosal glycosylation showed that gerbils respond in a similar way as humans and Rhesus monkeys which support gerbils to be a model suitable for studying H. pylori infection and disease outcome in relation to adherence.We studied the SSM mechanism of SabA phase variation and the cognate shift in sLex-binding phenotype and we show sLex-binding activity to be growth phase dependent. H. pylori vesicles were characterized for the major phosholipid and protein components. Virulence factors e.g., VacA, and CagA were identified and both the BabA and the SabA adhesins was shown to be located on the vesicle surface and to mediate specific binding to their cognate receptors present on the human gastric mucosa. H. pylori generate bacterial cells with different receptor binding phenotypes via the mechanisms of homologous recombination, SSM and nucleotide changes. These mechanisms will probably contribute to bacterial fitness by the generation of quasi species populations where some of the clones will be better adapted to the environmental chances during persistent infection.

sted, utgiver, år, opplag, sider
Umeå: Umeå university, 2009. s. 57
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1280
Emneord
H. pylori, adherence, BabA, SabA, Leb, sLex, phase variation, recombination, vesicles
Identifikatorer
urn:nbn:se:umu:diva-25931 (URN)978-91-7264-820-3 (ISBN)
Utgiver:
Oral mikrobiologi, 901 87, Umeå
Disputas
2009-10-09, KBC3A9, plan 3, KBC-huset, Umeå Universitet, Umeå, 09:00 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2009-09-21 Laget: 2009-09-13 Sist oppdatert: 2018-06-08bibliografisk kontrollert

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Bäckström, AnnaBorén, ThomasArnqvist, Anna

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