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dc.contributor.authorVyas, Heema KN
dc.contributor.authorIndraratna, Anuk D
dc.contributor.authorEverest-Dass, Arun
dc.contributor.authorPacker, Nicolle H
dc.contributor.authorDe Oliveira, David MP
dc.contributor.authorRanson, Marie
dc.contributor.authorMcArthur, Jason D
dc.contributor.authorSanderson-Smith, Martina L
dc.date.accessioned2021-06-08T00:31:00Z
dc.date.available2021-06-08T00:31:00Z
dc.date.issued2020
dc.identifier.issn2079-6382
dc.identifier.doi10.3390/antibiotics9110775
dc.identifier.urihttp://hdl.handle.net/10072/404967
dc.description.abstractGroup A Streptococcus (GAS) causes 700 million infections and accounts for half a million deaths per year. Antibiotic treatment failure rates of 20–40% have been observed. The role host cell glycans play in GAS biofilm formation in the context of GAS pharyngitis and subsequent antibiotic treatment failure has not been previously investigated. GAS serotype M12 GAS biofilms were assessed for biofilm formation on Detroit 562 pharyngeal cell monolayers following enzymatic removal of all N-linked glycans from pharyngeal cells with PNGase F. Removal of N-linked glycans resulted in an increase in biofilm biomass compared to untreated controls. Further investigation into the removal of terminal mannose and sialic acid residues with α1-6 mannosidase and the broad specificity sialidase (Sialidase A) also found that biofilm biomass increased significantly when compared to untreated controls. Increases in biofilm biomass were associated with increased production of extracellular polymeric substances (EPS). Furthermore, it was found that M12 GAS biofilms grown on untreated pharyngeal monolayers exhibited a 2500-fold increase in penicillin tolerance compared to planktonic GAS. Pre-treatment of monolayers with exoglycosidases resulted in a further doubling of penicillin tolerance in resultant biofilms. Lastly, an additional eight GAS emm-types were assessed for biofilm formation in response to terminal mannose and sialic acid residue removal. As seen for M12, biofilm biomass on monolayers increased following removal of terminal mannose and sialic acid residues. Collectively, these data demonstrate that pharyngeal cell surface glycan structures directly impact GAS biofilm formation in a strain and glycan specific fashion.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherMDPI
dc.relation.ispartofpagefrom775
dc.relation.ispartofissue11
dc.relation.ispartofjournalAntibiotics
dc.relation.ispartofvolume9
dc.relation.urihttp://purl.org/au-research/grants/NHMRC/APP1143266
dc.relation.grantIDAPP1143266
dc.relation.fundersNHMRC
dc.subject.keywordsScience & Technology
dc.subject.keywordsLife Sciences & Biomedicine
dc.subject.keywordsInfectious Diseases
dc.subject.keywordsPharmacology & Pharmacy
dc.subject.keywordsgroup A Streptococcus
dc.titleAssessing the Role of Pharyngeal Cell Surface Glycans in Group A Streptococcus Biofilm Formation
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationVyas, HKN; Indraratna, AD; Everest-Dass, A; Packer, NH; De Oliveira, DMP; Ranson, M; McArthur, JD; Sanderson-Smith, ML, Assessing the Role of Pharyngeal Cell Surface Glycans in Group A Streptococcus Biofilm Formation, Antibiotics, 2020, 9 (11), pp. 775
dcterms.dateAccepted2020-10-27
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/
dc.date.updated2021-06-08T00:18:57Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorPacker, Nicki
gro.griffith.authorEverest-Dass, Arun


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