Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/100353
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dc.contributor.authorHarvey, R.en
dc.contributor.authorTrappetti, C.en
dc.contributor.authorMahdi, L.en
dc.contributor.authorWang, H.en
dc.contributor.authorMcAllister, L.en
dc.contributor.authorScalvini, A.en
dc.contributor.authorPaton, A.en
dc.contributor.authorPaton, J.en
dc.date.issued2016en
dc.identifier.citationInfection and Immunity, 2016; 84(3):822-832en
dc.identifier.issn0019-9567en
dc.identifier.issn1098-5522en
dc.identifier.urihttp://hdl.handle.net/2440/100353-
dc.description.abstractStreptococcus pneumoniae is the leading infectious cause of death in children in the world. However, the mechanisms that drive the progression from asymptomatic colonization to disease are poorly understood. Two virulence-associated genomic accessory regions (ARs) were deleted in a highly virulent serotype 1 clinical isolate (strain 4496) and examined for their contribution to pathogenesis. Deletion of a prophage encoding a platelet-binding protein (PblB) resulted in reduced adherence, biofilm formation, reduced initial infection within the lungs, and a reduction in the number of circulating platelets in infected mice. However, the region's overall contribution to the survival of mice was not significant. In contrast, deletion of the variable region of pneumococcal pathogenicity island 1 (vPPI1) was also responsible for a reduction in adherence and biofilm formation but also reduced survival and invasion of the pleural cavity, blood, and lungs. While the 4496ΔPPI1 strain induced higher expression of the genes encoding interleukin-10 (IL-10) and CD11b in the lungs of challenged mice than the wild-type strain, very few other genes exhibited altered expression. Moreover, while the level of IL-10 protein was increased in the lungs of 4496ΔPPI1 mutant-infected mice compared to strain 4496-infected mice, the levels of gamma interferon (IFN-γ), CXCL10, CCL2, and CCL4 were not different in the two groups. However, the 4496ΔPPI1 mutant was found to be more susceptible than the wild type to phagocytic killing by a macrophage-like cell line. Therefore, our data suggest that vPPI1 may be a major contributing factor to the heightened virulence of certain serotype 1 strains, possibly by influencing resistance to phagocytic killing.en
dc.description.statementofresponsibilityRichard M. Harvey, Claudia Trappetti, Layla K. Mahdi, Hui Wang, Lauren J. McAllister, Alexandra Scalvini, Adrienne W. Paton, James C. Patonen
dc.language.isoenen
dc.publisherAmerican Society for Microbiologyen
dc.rightsCopyright © 2016, American Society for Microbiology. All Rights Reserved.en
dc.subjectLung; Animals; Humans; Mice; Streptococcus pneumoniae; Pneumococcal Infections; Bacterial Proteins; Interleukin-10; Virulence; Genomic Islands; Femaleen
dc.titleThe variable region of pneumococcal pathogenicity island 1 is responsible for unusually high virulence of a serotype 1 isolateen
dc.typeJournal articleen
dc.identifier.rmid0030041429en
dc.identifier.doi10.1128/IAI.01454-15en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/565526en
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1071659en
dc.identifier.pubid230013-
pubs.library.collectionMolecular and Biomedical Science publicationsen
pubs.library.teamDS10en
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidTrappetti, C. [0000-0001-8272-0068]en
dc.identifier.orcidMahdi, L. [0000-0002-5878-8385]en
dc.identifier.orcidPaton, J. [0000-0001-9807-5278]en
Appears in Collections:Molecular and Biomedical Science publications

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