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.pdfVIP

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.pdf

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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.pdf

Hindawi Publishing Corporation Comparative and Functional Genomics Volume 2009, Article ID 914762, 16 pages doi:10.1155/2009/914762 Research Article 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 Cristi L. Galindo,1, 2 Scott T. Moen,1 Elena V. Kozlova,1 Jian Sha,1 Harold R. Garner,2 Stacy L. Agar,1 and Ashok K. Chopra1 1 Department of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX 77555-1070, USA 2 Virginia Bioinformatics Institute, Virginia Polytechnic and State University, Blacksburg, VA 24061, USA Correspondence should be addressed to Ashok K. Chopra, achopra@ Received 26 July 2009; Revised 28 September 2009; Accepted 18 October 2009 Recommended by Antoine Danchin We 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 (Δlpp) 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 Δlpp 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

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