Transcriptomic analysis of the host circulating leukocyte response to infestation with the ectoparasitic mite Psoroptes ovis
Ontology highlight
ABSTRACT:
ORGANISM(S): Ovis aries
SUBMITTER: Stewart Burgess
PROVIDER: E-TABM-1193 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Transcriptional analysis of ovine skin response to infection with the parasitic mite Psoroptes ovis using the Agilent ovine transcriptome microarray platform. The results of statistical analysis (differential gene expression across the time course of infection was determined using a one way-analysis of variance (ANOVA) with a Student-Newman-Keuls (SNK) post-hoc test in Genespring GX 11.0 (Agilent Technologies, UK) comparing each of the 5 time points, non-infected and 1, 3, 6 and 24 hours post infection. Multiple test correction was performed using the Benjamini & Hochberg False Discovery Rate (FDR) procedure with an FDR corrected p-value cut-off set at 0.05) and fold change analysis (Fold change analysis was performed on the one-way anova dataset, probes with a fold change greater than 2 between any of the conditions were carried forward) are in archive E-TABM-1012.additional.zip. Quality control: Six biological replicates (sheep, n=6), multiple biopsies pooled from each animal at each time point of infection. Pooled samples from each sheep at each time point hybridised in single-dye (Cy3) format to Agilent ovine arrays. Positive and negative control probes utilised to assess array QC and real time qRT-PCR validation of selected array probes
2010-08-01 | E-TABM-1012 | biostudies-arrayexpress
Project description:Sub-thalamic deep brain stimulation (DBS) reversibly modulates ParkinsonM-bM-^@M-^Ys disease (PD) motor symptoms, providing an unusual opportunity to compare leukocyte transcripts in the same subjects before and after neurosurgery and after disconnecting the stimulus (ON-and OFF-stimulus). Here, we report rapid stimulus-induced and largely reversible changes in PD leukocyte transcripts, which were larger in scope than the disease-induced changes. These transcript changes classified advanced pre- from post-surgery PD patients and discriminated patients from controls. Moreover, the extent of changes correlated with the neurological efficacy of the DBS neurosurgery, and covered both regulatory pathways and individual transcript changes, e.g. SNCA, PARK7 and the splicing factor SFRS1. Following 1 hour OFF-stimulus, these changes were largely reversed. We extracted from these differences a modified transcripts signature which discriminated controls from advanced PD patients, pre- from post-surgery and ON-from OFF-stimulus conditions. A further gene-list independent analysis detected reversed pathways. Our findings suggest future uses of this approach and the discovered molecular signature for early diagnostics of PD and for identifying novel targets for therapeutic intervention in this and other DBS-treatable neurological diseases. 27 Total samples were analyzed. Study design included four conditions. PD patients (n=7) leukocyte blood samples were examined at 3 time points, and healthy control subjects (n=6) were examined once each. Samples were taken 1 day prior to sub-thalamic nucleous (STN) DBS treatment, several months after STN-DBS treatment upon optimal stimulation and following one hour electrical stimulation cessation. The off stimulation caused recruitment of the disease symptoms as measured by the Unified Parkinson's Disease Rating Scale motor section (UPDRS-III). The different stages are designated: S1 (pre-treatment), S2 (post STN-DBS) and S3 (upon off stimulation). All patients were on dopamine replacement therapy (DRT) when examined pre- and post-DBS off stimulation (albeit with reduced therapy dose post-DBS). To reduce biological variability among the samples which is not related to the study, only male subjects were included in this study. Samples from six age- and gender- matched healthy control subjects served to detect disease modified transcripts and for pre- and post- treatment comparisons. The study was approved by the human review board at the Hadassah University Hospital, Ein-Kerem (no. 6-07.09.07) in accordance with the Declaration of Helsinki. All study participants signed informed consent.
2012-01-09 | E-GEOD-23676 | biostudies-arrayexpress
Project description:To date, a variety of studies have employed gene expression profiling to classify ovarian carcinomas in clinically relevant subtypes. These studies provided valuable first clues to molecular changes in ovarian cancer that might be exploited in new treatment strategies. However, most studies were of relatively limited size and the number of overlapping genes in the identified profiles was minimal. Although identification of gene expression profiles associated with clinically relevant subtypes in ovarian cancer is important, knowledge is now emerging rapidly on how genes interact in pathways, networks and complexes; this allows us to unravel those cellular pathways determining the biological behavior of ovarian cancer, that might be successfully targeted with drugs. The aim of our study was: 1) To develop a gene expression profile associated with overall survival in advanced stage serous ovarian cancer, 2) to assess the association of pathways and transcription factors with overall survival, and 3) to validate our identified profile and pathways/transcription factors in an independent set of ovarian cancers. According to a randomized design, profiling of 157 advanced stage serous ovarian cancers was performed in duplicate using ~35K 70-mer oligonucleotide microarrays. A continuous predictor of overall survival was built taking into account well-known issues in microarray analysis, such as multiple testing and overfitting. A functional class scoring analysis was utilized to assess pathways/transcription factors for their association with overall survival. The prognostic value of genes that constitute our overall survival profile was validated on a fully independent, publicly available data set of 118 well-defined primary serous ovarian cancers. Furthermore, functional class scoring analysis was also performed on this independent data set to assess the similarities with results from our own data set. An 86-gene overall survival profile discriminated between patients with unfavorable and favorable prognosis (median survival, 19 vs. 41 months, respectively; permutation p-value of log-rank statistic = 0.015) and maintained its independent prognostic value in multivariate analysis. Genes that comprised the overall survival profile were also able to discriminate between the two risk groups in the independent data set. In our dataset 17/167 pathways and 13/111 transcription factors were associated with overall survival of which 16 and 12 respectively were confirmed in the independent dataset. Our study provides new clues to genes, pathways and transcription factors which contribute to the clinical outcome of serous ovarian cancer and might be exploited in designing new treatment strategies. Keywords: Oncology/Gynecological Cancers, Genetics and Genomics/Cancer Genetics, Genetics and Genomics/Gene Expression, Genetics and Genomics/Genomics According to a randomized design, profiling of 157 advanced stage serous ovarian cancers was performed in duplicate using ~35K 70-mer oligonucleotide microarrays. Two randomly selected samples were hybridized together on the arrays for intensity-based instead of ratio-based analysis of the microarray data.
2008-12-10 | E-GEOD-13876 | biostudies-arrayexpress
Project description:Phosgene is a lung damaging chemical warfare agent which can cause death by the inhalation route. In this study the inflammatory response to phosgene was mapped over a 96h time-course using a custom microarray in the Balb/c mouse. Three groups of six mice were exposed to phosgene and a three groups exposed to an air only control. Following exposure mice were culled at 6 timepoints (1, 4, 7, 24, 48 and 96h). RNA was extracted and run on the custom array.
2011-03-01 | E-GEOD-17249 | biostudies-arrayexpress
Project description:Francisella tularensis may enter the body thorugh the lungs and cause fatal infection. In this study the inflammatory response to the virulent strain of Francisella (Schu4) was mapped over a 96h time-course using a custom microarray. Six groups of 4 mice were exposed to aerosolised Francisella tularensis and a three groups exposed to vehicle only control (media only). Following exposure mice were culled at 4 timepoints (1, 24, 48 and 96h). RNA was extracted and run on the custom array.
2011-03-01 | E-GEOD-17248 | biostudies-arrayexpress
Project description:The toxin ricin has been shown to cause inflammatory lung damage, leading to pulmonary oedema and, at higher doses, mortality. In order to understand the genetic basis of this inflammatory cascade a custom microarray platform (1509 genes) directed towards immune and inflammatory markers was used to investigate the temporal expression profiles of genes in a Balb/c mouse model of inhalational ricin exposure. To facilitate examination of those genes involved in both inflammatory cascades and wound repair the dose which was investigated was sub-lethal across a 96 hour time course. Histopathology of the lung was mapped across the time course and genetic responses considered in the context of overall lung pathology. 685 genes were found to be statistically significantly different compared to controls, across the time course and these genes have been investigated in the context of their biological function in ricin poisoning. As well as confirming key inflammatory markers associated with ricin intoxication (TNFa and Il1b) several pathways that are altered in expression were identified following pulmonary exposure to ricin. These genes included those involved in cytokine-cytokine signalling cascades (IL1, IL1r, IL1r2, Ccl 4, 6, 10), focal adhesion (Fn1, ICAM1) and tissue remodelling (VEGF, Pim1). Furthermore, the observed alteration in expression of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) indicates a key role in membrane integrity and cellular adhesion in ricin poisoning. Data captured using this transcriptomic approach could be used to develop a specific approach to the treatment of inhalational ricin exposure. This work was conducted as part of a wider programme of work to compare a number of militarily relevant lung damaging agents, with a view to establishing a rational basis for the identification of more generic medical countermeasures. Four groups of six mice were exposed to ricin and a further groups exposed to vehicle only control (PBS). Following exposure mice were culled at 6 timepoints (1, 4, 7, 24, 48 and 96h). RNA was extracted and run on the custom array.
2009-08-19 | E-GEOD-17431 | biostudies-arrayexpress
Project description:The widespread commercial use of TiO2-NPs, such as in medical stents, has led to extensive investigations on their toxicity and biological impact but lacks a detailed study on their effects. Proteomics and transcriptomics are key methodologies to unravel cellular dynamics, macromolecular interactions and biological response to NP exposure through the protein or gene identification and quantification. We focus on integration of several Omics strategies that could offer a more complex understanding of the impact. In this study, our goal was to gain insight into the cellular response after the exposure to sublethal concentration of TiO2-ultra small nanoparticles (USNPs) and NPs by analyzing the modification on the genomic and proteomic expression in human microdermal endothelial cells (HMEC-1). We investigated the correlation between the NP size and the cellular response to the exposure. We evaluated if multiOmics approaches could thus reveal more extensive information on the potential cellular responses to NPs exposure.
2019-01-16 | PXD005359 | Pride
Project description:Maternal smoking has a severe negative effect on all stages of pregnancy that in consequence impairs fetal growth and development. Tobacco smoke-related defects are well established at the clinical level; however, little is known about molecular mechanisms underlying these pathological conditions. We thus employed a genomic approach to determine transcriptome alterations induced by maternal smoking in pregnancy. We assayed gene expression profiles in peripheral blood (M) leukocytes and placentas (PL) of pregnant smokers and those without significant exposure, and in cord blood (D) leukocytes of their babies. Comparative analyses defined significant deregulation of 193 genes in M cells, 329 genes in placentas, and 49 genes in D cells of smokers. These genes were mainly involved in xenobiotic metabolism, oxidative stress, inflammation, immunity, hematopoiesis, trophoblast differentiation, and vascularization. Functional annotation of the deregulated genes outlined processes and pathways affected by tobacco smoke. In smoker newborns, we identified several deregulated pathways associated with autoimmune diseases. The study demonstrates a limited ability of placenta to modulate toxic effects of maternal tobacco use at the gene expression level. Blood and placental samples were obtained from 91 women who gave birth to a baby in the Ceske Budejovice Hospital from November 2008 to March 2009. The study was approved by the Local Institutional Review Board. All participants provided written informed consent and completed an extensive questionnaire on pregnancy history (medication, diseases), delivery course, newborn characteristics and life style (smoking, diet, alcohol drinking, area of residency). Only subjects who underwent vaginal delivery were included in the study. Based on smoking history, the women were divided into two groups, “smokers” (N=20) and “non-smokers” (N=52), while passive smokers (N=19) were excluded from the study. Smoking status was further confirmed by detection of excessive plasma levels of cotinine (the major nicotine metabolite) in maternal blood.
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2013-03-25 | E-MEXP-3110 | biostudies-arrayexpress
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2013-05-02 | E-GEOD-45629 | biostudies-arrayexpress