{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["Claude Lachance"],"study_type":["transcription profiling by array"],"organism":["Mus musculus"],"species":["Mus musculus"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-GEOD-45862"],"description":["Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2-/-) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2-/- mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2-/- mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain. Total RNA obtained from spleen of C57BL/6 mice or C57BL/6 TLR2-KO mice infected with Streptococcus suis strain SC84. Four replicates in both groups."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Sample Treatment - Mice (C57BL/6 and C57BL/6 TLR2-KO) were infected for 6h with 5 x 10^7 CFU of Streptococcus suis strain SC84.","Scaning - Standard Illumina scanning protocol","Labeling - Biotinylated cRNA were prepared with the Ambion MessageAmp kit for Illumina arrays","Growth Protocol - Bacterial culture was prepared by transferring 10 M-NM-<l of 1/1,000 dilutions of 8-h cultures into 30 ml of THB, which was incubated for 16 h at 37M-0C without agitation. Stationary-phase bacteria were washed twice in PBS (pH 7.3). The bacterial pellet was then resuspended and adjusted to a concentration of 5 M-CM-^W 10^8 c.f.u. ml-1.","Hybridization - Standard Illumina hybridization protocol","Nucleic Acid Extraction - RNA was homogenized from RNAlater-stabilized spleen tissus, extracted and DNAse I treated using QIAGEN RNeasy mini kit in accordance with the prescribed protocol provided with the kit. Quality control was performed with Agilent Bioanalyser."],"figure_sub":["MIAME Score","Organization","Assays and Data","Processed Data","MAGE-TAB Files","Array Designs"],"pubmed_authors":["Claude Lachance","Marcelo Gottschalk","Mariela Segura","Jianguo Xu","PehuM-CM-)n Gerber"],"data_protocol":["Data Transformation - The data were first raw-filtered in order to identify and remove probesets that were not detected and then normalised using robust spline normalization with FlexArray v1.6 ID_REF =  VALUE = robust spline normalized"],"additional_accession":[]},"is_claimable":false,"name":"Genome wide analysis of C57BL-6 mice and C57BL/6 TLR2-KO mice infected with Chinese strain (SC84) of Streptococcus suis","description":"Streptococcus suis is an emerging zoonotic agent causing meningitis and septicemia. Outbreaks in humans in China with atypical cases of streptococcal toxic shock-like syndrome have been described to be caused by a clonal epidemic S. suis strain characterized as sequence type (ST) 7 by multilocus sequence typing, different from the classical ST1 usually isolated in Europe. Previous in vitro studies showed that Toll-like receptor (TLR) 2 plays a major role in S. suis ST1 interactions with host cells. In the present study, the in vivo role of TLR2 in systemic infections caused by S. suis ST1 or ST7 strains using TLR2 deficient (TLR2-/-) mice was evaluated. TLR2-mediated recognition significantly contributes to the acute disease caused by the highly virulent S. suis ST1 strain, since the TLR2-/- mice remained unaffected when compared to wild type (WT) mice. The lack of mortality could not be associated with a lower bacterial burden; however, a significant decrease in the induction of pro-inflammatory mediators, as evaluated by microarray, real-time PCR and protein assays, was observed. On the other hand, TLR2-/- mice infected with the epidemic ST7 strain presented no significant differences regarding survival and expression of pro-inflammatory mediators when compared to the WT mice. Together, these results show a TLR2-independent host innate immune response to S. suis that depends on the strain. Total RNA obtained from spleen of C57BL/6 mice or C57BL/6 TLR2-KO mice infected with Streptococcus suis strain SC84. Four replicates in both groups.","dates":{"release":"2013-06-01T00:00:00Z","modification":"2023-08-27T11:55:41.464Z","creation":"2022-01-31T17:34:51.726Z"},"accession":"E-GEOD-45862","cross_references":{"GEO":["GSE45862"],"EFO":["EFO_0002768"]}}