E-GEOD-6810 - Transcription profiling of mouse splenocytes response to infection with wild type or virB mutant Brucella strains
Submitted on 19 January 2007, released on 6 November 2008, last updated on 27 March 2012
The virB operon, encoding a Type IV secretion system (T4SS), is essential for intracellular survival and persistent infection of Brucella spp. To better understand the role of the T4SS in evading host defense mechanisms and establishing chronic infection, we compared transcriptional profiles of the host response to infection with wild type Brucella strains and strains that fail to express the virB genes. Analysis of host gene expression profiles three days after inoculation with wild type Brucella strains revealed an inflammatory response dominated by interferon-induced genes. This analysis found that not only the type II but also type I interferon pathway was elicited by Brucella infection. Real time RT-PCR showed that a group of genes from these pathways was induced by day 3 post-infection and declined to baseline levels by day 7. In contrast, neither of the two virB mutant strains elicited expression of interferon-induced genes, demonstrating that the T4SS was required to trigger an inflammatory response early during infection. Experiment Overall Design: We performed microarray-based expression analyses of splenocytes from mice infected with two virulent strains (B. abortus 2308 and B. melitensis 16M), and two different B. abortus virB mutants, whose virB operon was either disrupted (BA41) or completely deleted (ADH4.2), to better understand the contribution of the T4SS in establishing infection of the reticuloendothelial system. 3 days after infection of mice, spleens were excised for RNA extraction. For each bacterial strain, RNA from 5 mice was pooled and reverse transcribed for hybridization to an array. Each experiment was performed in duplicate.
transcription profiling by array, disease state, individual genetic characteristics
Brucella requires a functional Type IV secretion system to elicit innate immune responses in mice. Christelle M Roux, Hortensia G Rolán, Renato L Santos, Phillip D Beremand, Terry L Thomas, L Garry Adams, Renée M Tsolis.