Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female CBA mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice
Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female C57BL/6 mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice
Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female C57BL/6 mice using genome-wide expression profiling and temporal analysis to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in GBS UTI in mice over time and in UPEC UTI in mice at 24h
Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female CBA mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice Whole mouse bladder collected at 2h following transurethral infection for RNA extraction and hybridization on Affymetrix microarrays. Non-pooled samples were used, with one array per mouse to expand power of expression profiles. Control mice received only PBS as a mock infection. Group sizes were five mice per group, and therefore five arrays were used per group.
Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female C57BL/6 mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice Whole mouse bladder collected at 2h following transurethral infection for RNA extraction and hybridization on Affymetrix microarrays. Non-pooled samples were used, with one array per mouse to expand power of expression profiles. Control mice received only PBS as a mock infection. Group sizes were five mice per group, and therefore five arrays were used per group.
Project description:A strain of UPEC CFT073 lacking the three known NO detoxifiaction mechanisms, Hmp, FlRd and Nrf is used to study the global effect of NO on the pathogen
Project description:Ascending bacterial infections of the male genitourinary tract by Escherichia coli are an important cause of male infertility. Thus understanding mechanisms by which immunocompetent cells such as testicular macrophages (TM) respond to infection and how bacterial pathogens manipulate defense pathways is of great relevance. Following infection with uropathogenic E. coli (UPEC) whole genome expression profiling revealed induction of the calcium-dependent nuclear factor of activated T cells (NFAT) signaling pathway in TM as well as in peritoneal macrophages (PM) that were used in comparison. UPEC-dependent NFAT activation was confirmed in cultured TM and in TM using an in vivo infection model. Elevated expression of NFATC2-regulated anti-inflammatory cytokines was found in TM (IL-4, IL-13) and PM (IL-3, IL-4, IL-13). NFATC2 is activated by a rapid influx of calcium caused by the UPEC pore forming toxin alpha-hemolysin. Mutant analysis identified alpha-hemolysin as the main virulent factor responsible for UPEC-dependant suppression of IL-6 and TNF-a cytokine release from PM. Alpha-hemolysin caused differential activation of MAP kinase and AP-1 signaling pathways in TM and PM leading to differential expression profiles of key pro-inflammatory cytokines in PM (IL-1a, IL-1b and IL-6 downregulated) and TM (IL-1b and IL-6 upregulated). In contrast to PM, treatment with lipopolysaccharide did not result in activation of the NFkB pathway in TM as shown by lack of degradation of IkBa and lack of pro-inflammatory cytokine secretion (IL-6, TNF-a). In conclusion, these results propose a mechanism how TM can defend against microbes, while at the same time they are able to maintain the immune privileged status of the testis. 2 Macrophage populations ( peritoneal, testicular) infected with UPEC CFT073; timepoints of mrna harvest at 0 min (control), 30 min and 60 min; of each point 2 biological replicates; of each repliccate 2 technical replicates: summa summarum: 2*((1+1+1)*2*2)=24 samples