Helicobacter pylori SabA adhesin in persistent infection and chronic inflammation.
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ABSTRACT:
SUBMITTER: Mahdavi J
PROVIDER: S-EPMC2570540 | biostudies-literature | 2002 Jul
REPOSITORIES: biostudies-literature
Publications
Helicobacter pylori SabA adhesin in persistent infection and chronic inflammation.
Mahdavi Jafar J Sondén Berit B Hurtig Marina M Olfat Farzad O FO Forsberg Lina L Roche Niamh N Angstrom Jonas J Larsson Thomas T Teneberg Susann S Karlsson Karl-Anders KA Altraja Siiri S Wadström Torkel T Kersulyte Dangeruta D Berg Douglas E DE Dubois Andre A Petersson Christoffer C Magnusson Karl-Eric KE Norberg Thomas T Lindh Frank F Lundskog Bertil B BB Arnqvist Anna A Hammarström Lennart L Borén Thomas T
Science (New York, N.Y.) 20020701 5581
Helicobacter pylori adherence in the human gastric mucosa involves specific bacterial adhesins and cognate host receptors. Here, we identify sialyl-dimeric-Lewis x glycosphingolipid as a receptor for H. pylori and show that H. pylori infection induced formation of sialyl-Lewis x antigens in gastric epithelium in humans and in a Rhesus monkey. The corresponding sialic acid-binding adhesin (SabA) was isolated with the "retagging" method, and the underlying sabA gene (JHP662/HP0725) was identified. ...[more]
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Project description:BackgroundGastric Helicobacter pylori colonization leads to iron deficiency anemia (IDA), especially in children and adolescents. However the pathogenesis is poorly understood.ObjectiveWe sought to identify specific H. pylori genes involved in IDA development, by comparing bacterial genome-wide expression profiling in patients affected or not.MethodsH. pylori were isolated from four children with IDA and four from matched controls without IDA. Based on these isolates, cDNA microarrays under iron-replete or depleted conditions were systematically performed to compare gene expression profiles at the whole genome level. Real-time reverse-transcription (RT-) PCR and protein assays were performed for further assessing the profile differentiation of the identified H. pylori IDA-associated genes.ResultsWe identified 29 and 11 genes with significantly higher or lower expression in the IDA isolates compared to non-IDA isolates, respectively. Especially notable were higher expression of sabA gene encoding sialic acid-binding adhesin in the IDA isolates, which was confirmed by real-time RT-PCR study. Moreover, iron-depletion in vitro led to up-regulation of fecA1 and frpB1 genes and down-regulation of pfr, as predicted. Known iron-regulated genes such as fur, pfr, fecA, and feoB did not significantly differ between both groups. The IDA isolates had significantly higher expression of vacuolating cytotoxin gene vacA than non-IDA isolates, consistent with the results of VacA protein assays. There were no significant differences in bacterial growth value between IDA and non-IDA isolates.ConclusionsIt is likely that H. pylori carrying high expression of sabA causes IDA, especially in children and adolescents who have increased daily iron demand. In addition, it is possible that several host-interactive genes, including vacA, may play a synergistic role for sabA in IDA development.
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