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dc.contributor.authorGalindo, Cristi L.
dc.contributor.authorMoen, Scott T.
dc.contributor.authorKozlova, Elena V.
dc.contributor.authorSha, Jian
dc.contributor.authorGarner, Harold R.
dc.contributor.authorAgar, Stacy L.
dc.contributor.authorChopra, Ashok K.
dc.date.accessioned2017-09-18T10:00:29Z
dc.date.available2017-09-18T10:00:29Z
dc.date.issued2010-01-20
dc.identifier.citationCristi L. Galindo, Scott T. Moen, Elena V. Kozlova, et al., “Comparative Analyses of Transcriptional Profiles in Mouse Organs Using a Pneumonic Plague Model after Infection with Wild-Type Yersinia pestis CO92 and Its Braun Lipoprotein Mutant,” Comparative and Functional Genomics, vol. 2009, Article ID 914762, 16 pages, 2009. doi:10.1155/2009/914762
dc.identifier.urihttp://hdl.handle.net/10919/79052
dc.description.abstractWe employed Murine GeneChips to delineate the global transcriptional profiles of the livers, lungs, and spleens in a mouse pneumonic plague infection model with wild-type (WT) Y. pestis CO92 and its Braun lipoprotein () mutant with reduced virulence. These organs showed differential transcriptional responses to infection with WT Y. pestis, but the overall host functional processes affected were similar across all three tissues. Gene expression alterations were found in inflammation, cytokine signaling, and apoptotic cell death-associated genes. Comparison of WT and mutant-infected mice indicated significant overlap in lipopolysaccharide- (LPS-) associated gene expression, but the absence of Lpp perturbed host cell signaling at critical regulatory junctions resulting in altered immune response and possibly host cell apoptosis. We generated a putative signaling pathway including major inflammatory components that could account for the synergistic action of LPS and Lpp and provided the mechanistic basis of attenuation caused by deletion of the lpp gene from Y. pestis in a mouse model of pneumonic plague.
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleComparative Analyses of Transcriptional Profiles in Mouse Organs Using a Pneumonic Plague Model after Infection with Wild-Type Yersinia pestis CO92 and Its Braun Lipoprotein Mutant
dc.typeJournal Article
dc.date.updated2017-09-18T10:00:29Z
dc.description.versionPeer Reviewed
dc.language.rfc3066en
dc.rights.holderCopyright © 2009 Cristi L. Galindo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.identifier.doihttps://doi.org/10.1155/2009/914762


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