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BabA-mediated adherence of pediatric ulcerogenic H. pylori strains to gastric mucins at neutral and acidic pH

dc.contributor.authorQuintana-Hayashi, Macarena P.
dc.contributor.authorRocha, Raquel
dc.contributor.authorPadra, Médea
dc.contributor.authorThorell, Anders
dc.contributor.authorJin, Chunsheng
dc.contributor.authorKarlsson, Niclas G.
dc.contributor.authorRoxo-Rosa, Mónica
dc.contributor.authorOleastro, Mónica
dc.contributor.authorLindén, Sara K.
dc.date.accessioned2019-03-20T17:59:53Z
dc.date.available2019-03-20T17:59:53Z
dc.date.issued2018
dc.description.abstractHelicobacter pylori infection can result in non-ulcer dyspepsia (NUD), peptic ulcer disease (PUD), adenocarcinoma, and gastric lymphoma. H. pylori reside within the gastric mucus layer, mainly composed of mucins carrying an array of glycan structures that can serve as bacterial adhesion epitopes. The aim of the present study was to characterize the binding ability, adhesion modes, and growth of H. pylori strains from pediatric patients with NUD and PUD to gastric mucins. Our results showed an increased adhesion capacity of pediatric PUD H. pylori strains to human and rhesus monkey gastric mucins compared to the NUD strains both at neutral and acidic pH, regardless if the mucins were positive for Lewis b (Leb), Sialyl-Lewis x (SLex) or LacdiNAc. In addition to babA positive strains being more common among PUD associated strains, H. pylori babA positive strains bound more avidly to gastric mucins than NUD babA positive strains at acidic pH. Binding to Leb was higher among babA positive PUD H. pylori strains compared to NUD strains at neutral, but not acidic, pH. PUD derived babA-knockout mutants had attenuated binding to mucins and Leb at acidic and neutral pH, and to SLex and DNA at acidic pH. The results highlight the role of BabA-mediated adherence of pediatric ulcerogenic H. pylori strains, and points to a role for BabA in adhesion to charged structures at acidic pH, separate from its specific blood group binding activity.pt_PT
dc.description.sponsorshipFCT-PTDC/BIM-MEC/1051/2012 grant from the Fundação para a Ciência e a Tecnologia (FCT)pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationVirulence. 2018;9(1):1699-1717. doi: 10.1080/21505594.2018.1532243pt_PT
dc.identifier.doi10.1080/21505594.2018.1532243pt_PT
dc.identifier.issn2150-5594
dc.identifier.urihttp://hdl.handle.net/10400.18/6254
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherTaylor & Francis Openpt_PT
dc.relation.publisherversionhttps://www.tandfonline.com/doi/full/10.1080/21505594.2018.1532243pt_PT
dc.subjectHelicobacetr pyloript_PT
dc.subjectAdherencept_PT
dc.subjectVirulencept_PT
dc.subjectMucinpt_PT
dc.subjectAdhesinpt_PT
dc.subjectBabApt_PT
dc.subjectBindingpt_PT
dc.subjectChildrenpt_PT
dc.subjectGlycosylationpt_PT
dc.subjectpHpt_PT
dc.subjectPeptic Ulcerpt_PT
dc.subjectVirulencept_PT
dc.subjectInfecções Gastrointestinaispt_PT
dc.titleBabA-mediated adherence of pediatric ulcerogenic H. pylori strains to gastric mucins at neutral and acidic pHpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FBIM-MEC%2F1051%2F2012/PT
oaire.citation.endPage1717pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage1699pt_PT
oaire.citation.titleVirulencept_PT
oaire.citation.volume9pt_PT
oaire.fundingStream3599-PPCDT
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication46fab5cc-442f-4ef1-a9e3-1ea2ec450999
relation.isProjectOfPublication.latestForDiscovery46fab5cc-442f-4ef1-a9e3-1ea2ec450999

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