Unknown,Transcriptomics,Genomics,Proteomics

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Pho regulon modulation of Enterohemorrhagic Escherichia coli O157:H7 virulence factors

ABSTRACT: In E. coli the phosphate homeostasis is regulated by the Pst system and the two-component system PhoB/R. Pathogens like E. coli O157:H7 are responsible for many outbreaks and can be found and survive in poor inorganic phosphate (Pi) environments. To understand global EHEC O157:H7 EDL933 strain responses to Pi-starvation, we compared the transcriptomes of EDL933 the WT strain grown in MOPS Pi rich medium and that grown in MOPS Pi poor medium, using the Affymetrix GeneChip® E. coli Genome 2.0 Array. Also we investigated the EDL933 global response to the absence of PhoB by comparing the transcriptomes of the WT strain the ΔphoB mutant both grown in Low Pi EDL933WT strain and its isogenic mutant ΔphoB were grown in Pi- and/or in Pi+ conditions until the OD600 reached respectively 0.55 to 0.6. Samples equal to 5.108 CFU were taken from this mid log phase and processed for transcriptomes analysis. Ten µg of RNAs were extracted and retro-transcripted. One µg of the fragmented and biotinylated cDNAs, were hybridized onto Affymetrix GeneChip® E. coli. The data were processed using the FlexArray® software; RMA normalization and the levels of transcription obtained from 3 biological replicates of each experimental condition were compared using the EB (Wright & Simon) algorithm. We then conducted comparisons between EDL933WT grown in Pi- and in Pi+ conditions (comparison A) and between EDL933WT and EDL933∆phoB strains both grown in Pi- (comparison B). The differentially expression conditions corresponded to 2-fold change (FC) cut-off and p-value < 0.05.

ORGANISM(S): Escherichia coli

SUBMITTER: Samuel Mohammed Chekabab

PROVIDER: E-GEOD-50529 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Resiquimod is a nucleoside analog belonging to the imidazoquinoline family of compounds which is known to signal through Toll-like receptor 7. Resiquimod treatment has been demonstrated to inhibit the development of allergen induced asthma in experimental models. Despite this demonstrated effectiveness, little is known about the molecular events responsible for this effect. The aim of the present study was to elucidate the molecular processes which were altered following resiquimod treatment and antigen challenge in a mouse model of allergic asthma. Employing microarray analysis, we have characterized the 'asthmatic' transcriptome of the murine lung and determined that it includes genes involved in: the control of cell cycle progression, airway remodelling, the complement and coagulation cascades, and chemokine signalling. We have demonstrated that systemic resiquimod administration resulted in the recruitment of NK cells to the lungs of the mice, although no causal relationship between NK cell recruitment and treatment efficacy was found. Furthermore, results of our studies demonstrated that resiquimod treatment resulted in the normalization of the expression of genes involved with airway remodelling and chemokine signalling, and in the modulation of the expression of genes including cytokines and chemokines, adhesion molecules, and B-cell related genes, involved in several aspects of immune function and antigen presentation. Overall, our findings identified several genes, important in the development of asthma pathology, that were normalized following resiquimod treatment thus improving our understanding of the molecular consequences of resiquimod treatment in the lung milieu. Experiment Overall Design: A total of 18 samples, from 6 sets of biological replicates, were analyzed. 9 A/J and 9 C57BL/6 mice were divided into three equal groups. All animals were sensitized to ovalbumin, one group received PBS aerosol challenges, the other two received 1% ovalbumin aerosol challenges. Of the two ovalbumin challenged groups, one recieved resiquimod 24hours before each challenge.

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Pho regulon modulation of Enterohemorrhagic Escherichia coli O157:H7 virulence factors

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Pho regulon modulation of Enterohemorrhagic *Escherichia coli* O157:H7 virulence factors

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Pho regulon modulation of Enterohemorrhagic Escherichia coli O157:H7 virulence factors