Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.micinf.2009.12.002
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dc.titleEvidence for an intact polysaccharide capsule in Bordetella pertussis
dc.contributor.authorNeo, Y.
dc.contributor.authorLi, R.
dc.contributor.authorHowe, J.
dc.contributor.authorHoo, R.
dc.contributor.authorPant, A.
dc.contributor.authorHo, S.
dc.contributor.authorAlonso, S.
dc.date.accessioned2011-07-26T06:52:46Z
dc.date.available2011-07-26T06:52:46Z
dc.date.issued2010
dc.identifier.citationNeo, Y., Li, R., Howe, J., Hoo, R., Pant, A., Ho, S., Alonso, S. (2010). Evidence for an intact polysaccharide capsule in Bordetella pertussis. Microbes and Infection 12 (3) : 238-245. ScholarBank@NUS Repository. https://doi.org/10.1016/j.micinf.2009.12.002
dc.identifier.issn12864579
dc.identifier.issn1769714X
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/24665
dc.description.abstractPolysaccharide capsules contribute to the pathogenesis of many bacteria species by providing resistance against various defense mechanisms. The production of a capsule in Bordetella pertussis, the etiologic agent of whooping cough, has remained controversial; earlier studies reported this pathogen as a capsulated microorganism whereas the recent B. pertussis genome analysis revealed the presence of a truncated capsule locus. In this work, using transmission electron microscopy and immunostaining approaches, we provide a formal evidence for the presence of an intact microcapsule produced at the surface of both laboratory strain and clinical isolates of B. pertussis. In agreement with previous studies, we found that the capsule is optimally produced in avirulent phase. Unexpectedly, the presence of the capsule was also detected at the surface of virulent B. pertussis bacteria. Consistently, a substantial transcriptional activity of the capsule operon was detected in virulent phase, suggesting that the capsular polysaccharide may play a role during pertussis pathogenesis. In vitro assays indicated that the presence of the capsule does not affect B. pertussis adherence to mammalian cells and does not further protect the bacterium from phagocytosis, complement-mediated killing or antimicrobial peptide attack. © 2009.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.micinf.2009.12.002
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentMICROBIOLOGY
dc.description.doi10.1016/j.micinf.2009.12.002
dc.description.sourcetitleMicrobes and Infection
dc.description.volume12
dc.description.issue3
dc.description.page238-245
dc.identifier.isiut000275843400009
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