Construction and characterisation of Bordetella pertussis mutants lacking the vir-regulated P.69 outer membrane protein

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Show simple item record Roberts, M. en_US Fairweather, N en_US Leininger, E en_US Pickard, D en_US Hewlett, E en_US Robinson, A en_US Hayward, C. en_US Dougan, G en_US Charles, Ian en_US
dc.contributor.editor en_US 2014-04-03T01:06:04Z 2014-04-03T01:06:04Z 1991 en_US
dc.identifier 2009007984 en_US
dc.identifier.citation Dougan, G et al. 1991, 'Construction and characterisation of Bordetella pertussis mutants lacking the vir-regulated P.69 outer membrane protein', Molecular Microbiology, vol. 5, no. 6, pp. 1393-1404. en_US
dc.identifier.issn 0950-382X en_US
dc.identifier.other C1UNSUBMIT en_US
dc.description.abstract The Bordetella pertussis P.69 protein is an immunogen with vaccine potential. The role of this protein in pathogenesis is unclear; it has been associated with the toxic adenylate cyclase and adhesion to eukaryotic cells. For further analysis of the role of P.69 in the biology of B. pertussis, we have constructed strains which specifically lack P.69. The cloned P.69 (prn) gene of B. pertussis was insertionally inactivated with a kanamycin-resistance cassette. This inactivated gene was used to construct P.69- mutants of B. pertussis by allelic exchange using plasmid pRTP1. B. pertussis P.69- strains produced normal levles of other vir-regulated factors, including adenylate cyclase. The serotype of B. pertussis, determined by Eldering and Preston typing sera and monoclonal antibodies, was also unaffected by the presence or absence of P.69. The ability of a prn mutant to adhere to and invade HEp2 cells was not significantly different from that of its parent strain. A strain containing a mutation in fhaB was significantly less adhesive and invasive than its parent, and a prn fhaB double mutant exhibited an even greater reduction in adhesiveness and invasiveness down to levels comparable with a Vir- strain. However, strains harbouring mutations in FHA and/or P.69 were able to colonize or multiply in the murine respiratory tract, although a Vir- strain was unable to survive and proliferate in the same infection model. en_US
dc.language en_US
dc.publisher Blackwell Publishing Ltd en_US
dc.relation.isbasedon en_US
dc.title Construction and characterisation of Bordetella pertussis mutants lacking the vir-regulated P.69 outer membrane protein en_US
dc.parent Molecular Microbiology en_US
dc.journal.volume 5 en_US
dc.journal.number 6 en_US
dc.publocation UK en_US
dc.identifier.startpage 1393 en_US
dc.identifier.endpage 1404 en_US SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 090300 en_US
dc.personcode 0000061553 en_US
dc.personcode 0000060171 en_US
dc.personcode 0000060178 en_US
dc.personcode 0000060143 en_US
dc.personcode 0000064156 en_US
dc.personcode 0000064157 en_US
dc.personcode 0000082203 en_US
dc.personcode 0000060138 en_US
dc.personcode 109028 en_US
dc.percentage 100 en_US Biomedical Engineering en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US en_US
dc.location.activity en_US
dc.staffid 109028 en_US

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