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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Galectin-8 downmodulates TLR4 activation and impairs bacterial clearance in a mouse model of Pseudomonas keratitis

ABSTRACT: In our study, we used a mouse model infected with Pseudomonas aeruginosa (PA) to provoke a painful, sight-threatening corneal infection. FACS sorted WT and Gal-8-/- neutrophils of PA infected corneas were processed for next-generation transcriptomic RNA sequencing (RNA-seq).

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Microcebus murinus

SUBMITTER: Abdulraouf Ramadan

PROVIDER: E-MTAB-12376 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Semi-quantitative proteomics enables mapping of global neutrophil dynamics following influenza virus infection

Project description:Lung neutrophils are causally associated with IAV-induced disease severity. Less is known about the repertoire of lethal IAV-associated neutrophil proteins or about how global changes in different neutrophil compartments are coordinated following lethal IAV infection. Here, we use semi-quantitative proteomics to characterize dynamic alterations in BM, blood and lung neutrophils at homeostasis or following a lethal IAV infection, with a secondary aim of identifying lung neutrophil-derived proteins which are selectively induced following IAV infection. Our findings identify bone marrow neutrophil maturation as the key site of anti-viral activity induction, with further upregulation or release of both anti-viral and antimicrobial effectors occurring following lung tissue infiltration.

2019-05-29 | PXD012681 | Pride

Global DNA methylation changes and differential gene expression in Anaplasma phagocytophilum-infected human neutrophils

Project description:Background: Anaplasma phagocytophilum is an obligate intracellular prokaryotic pathogen that both infects and replicates within human neutrophils. The bacterium represses multiple antimicrobial functions while simultaneously increasing proinflammatory functions by reprogramming the neutrophil genome. Previous reports show that many observed phenotypic changes are in part explained by altered gene transcription. We recently identified that large chromosomal regions of the neutrophil genome are differentially expressed during A. phagocytophilum infection. Because of this, we sought to determine whether gene expression programs altered by infection were the result of changes in the host neutrophil DNA methylome. Results: Within 24 h of infection, marked increases in DNA methylation were observed genome-wide as compared with mock-infected controls and pharmacologic inhibition of DNA methyltransferases resulted in decreased bacterial growth. New regions of DNA methylation were enriched at intron and exon junctions; however, intragenic methylation did not correlate with altered gene expression. In contrast, intergenic DNA methylation was associated with A. phagocytophilum-induced gene expression changes. Within the major histocompatibility complex locus on chromosome 6, a region with marked changes in infection-induced differential gene expression, new regions of methylation were localized to boundaries of active and inactive chromatin. Conclusions: These data strongly suggest that A. phagocytophilum infection, in addition to altering histone structure, alters DNA methylation and the epigenome of its host cell to promote survival and replication, providing evidence that such bacterial infection can radically alter the epigenome of its host cell. Examination of methylated DNA sites in 3 human donors' neutrophils with and without 24h infection by Anaplasma phagocytophilum.

2015-09-22 | E-GEOD-73228 | biostudies-arrayexpress

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-01 | E-GEOD-52840 | biostudies-arrayexpress

Expression data from control, aged and activated neutrophils in mouse blood

Project description:Neutrophils provide immune protection against pathogens but also may promote tissue injury in inflammatory diseases. Although neutrophils are generally considered as a relatively homogeneous population, evidence for heterogeneity is emerging. Under steady-state conditions, neutrophil heterogeneity may arise from ageing and the replenishment by newly released neutrophils from the bone marrow. We used microarray to globally analyze gene expression in aged neutrophils and characterize the inflammatory programs that are activated during the aging process in the circulation. Control, aged and activated neutrophils were sorted directly from mouse blood for RNA extraction and hybridization on Affymetrix microarrays. We transfused whole blood and harvested donor neutrophils marked by the CD45.1 allele 6h later to derive neutrophils that had truly aged in vivo. Sorted neutrophils were compared to control donor neutrophils that had been transferred for only 10 min. Additionally, we harvested circulating neutrophils from TNF-? treated mice for comparison with neutrophils activated by systemic inflammation.

2015-09-24 | E-GEOD-69886 | biostudies-arrayexpress

HiRIEF TMT Proteomics of Arabidosis thaliana, wildtype versus oligopeptidases' KO mutants

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2018-11-14 | PXD009651 | Pride

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development [ChIP-Seq]

Project description:In immune responses, activated T cells migrate to B cell follicles and develop to T follicular helper (Tfh) cells, a new subset of CD4+ T cells specialized in providing help to B lymphocytes in the induction of germinal centers 1-3. Although Bcl6 has been shown to be essential in Tfh cell function, it may not regulate the initial migration of T cells 4 or the induction of Tfh program as exampled by CXCR5 upregulation 5. Here, we show that the Achaete-Scute homologue 2 (Ascl2) gene that encodes a basic helix-loop-helix (bHLH) transcription factor 6, is selectively upregulated in its expression in Tfh cells. Ectopic expression of Ascl2 uniquely upregulates CXCR5 but not Bcl6 and downregulates CCR7 expression in T cells in vitro and accelerates T cell migration to the follicles and Tfh cell development in vivo. Combined transcriptome profiling and genome-wide occupancy analysis indicate that Ascl2 directly regulates Tfh-related genes while inhibits expression of Th1 and Th17 genes. Acute deletion of Ascl2 as well as blockade of its function with the Id3 protein in peripheral CD4+ T cells results in a failure in Tfh cell development and the germinal center response. Conversely, mutation of Id3, known to cause antibody-mediated autoimmunity, greatly enhances Tfh cell generation. Thus, Ascl2 critically and directly initiates Tfh cell development. Decide Ascl2 binding sites in CD4+ T cells

2014-01-01 | E-GEOD-52839 | biostudies-arrayexpress

MiRNAs 182 and 183 are necessary to maintain adult cone photoreceptor outer segments and visual function

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-20 | E-GEOD-58501 | biostudies-arrayexpress

Transcription factor Achaete-Scute homologue 2 initiates T follicular helper cell development [array]

2014-01-01 | E-GEOD-52838 | biostudies-arrayexpress

Expression data of wild type and C-DGCR8 KO cones at different timepoints [RNA-seq]

Project description:We have analyzed gene expression in cone photoreceptors isolated from wild type and C-DGCR8 (DiGeorge Syndrome Critical Region Gene 8) KO mice at five different time points to get a mechanistic inside into the altered molecular pathways after microRNAs depletion. Cones were isolated by FACS from wild type and C-DGCR8 KO mice expressing Cre recombinase postnatally specifically in cones (D4-Cre) and bearing conditional null Dgcr8 allele. Experiments were performed in duplicates from different time points (P30, P40, P50, P60, and P90). Total RNA was extracted and next-generation RNA sequencing was performed.

2014-06-20 | E-GEOD-58498 | biostudies-arrayexpress

Expression data of wild type and C-DGCR8 KO cones at different timepoints [array]

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