NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE22299 Query DataSets for GSE22299
Status Public on Dec 07, 2010
Title Role of the Yersinia pestis Virulence Plasmid in Evading a Protective Polymorphonuclear Leukocyte Response During the Early Stages of Bubonic Plague
Organism Rattus norvegicus
Experiment type Expression profiling by array
Summary A delay in the mammalian inflammatory response is a prominent feature of infection with Yersinia pestis, the agent of bubonic and pneumonic plague. Y. pestis factors have been identified that either do not stimulate a normal inflammatory response, or actively suppress it. Prominent among these are components of the Type III secretion system that is encoded on the Yersinia virulence plasmid (pYV). We used a rat model of bubonic plague to characterize the kinetics and extent of the mammalian transcriptomic response to infection with wild-type or pYV-negative Y. pestis in the draining lymph node. Remarkably, dissemination and multiplication of wild-type Y. pestis during the bubonic stage of disease did not induce any detectable gene expression response by host lymph node cells. This was followed, however, by an extensive transcriptomic response, including upregulation of several cytokine, chemokine, and other immune response genes, after systemic spread during septicemic plague. Matched lymph node samples used for histopathology and extracellular cytokine measurements, combined with the microarray data set, broadly outlined the mammalian immune response to Y. pestis and how it is influenced by pYV-encoded factors. The results indicate that both WT and pYV– Y. pestis induce primarily a Th17 response, and not a Th1 or Th2 response. In the absence of pYV, a sustained recruitment of polymorphonuclear leukocytes, the major Th17 effector cell, to the lymph node resulted in clearance of infection. Thus, the ability to counteract a Th17- driven PMN response in the lymph node appears to be a major function of the Y. pestis virulence plasmid. In contrast, classic markers of the proinflammatory response and macrophage activation, such as TNF-á and IFN-ã, were not induced at all by pYV– Y. pestis, and appeared only late in infection with WT Y. pestis.
 
Overall design Rats treated with PBS and Yersinia pestis at various time points.
 
Contributor(s) Comer JE, Sturdevant DE, Carmody AB, Virtaneva K, Gardner D, Long D, Porcella SF, Hinnebusch BJ
Citation(s) 20876291
Submission date Jun 10, 2010
Last update date Jul 31, 2017
Contact name Dan Sturdevant
E-mail(s) dsturdevant@niaid.nih.gov
Phone 4063639248
Organization name NIH
Department NIAID
Lab RTS
Street address 903 S 4th street
City Hamilton
State/province MT
ZIP/Postal code 59840
Country USA
 
Platforms (1)
GPL1355 [Rat230_2] Affymetrix Rat Genome 230 2.0 Array
Samples (50)
GSM555054 Rat treated with PBS 36hr, rep 1
GSM555055 Rat treated with PBS 36hr, rep 2
GSM555056 Rat treated with PBS 36hr, rep 3
Relations
BioProject PRJNA127391

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE22299_RAW.tar 134.9 Mb (http)(custom) TAR (of CEL, CHP)
Processed data included within Sample table
Processed data provided as supplementary file
| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap