ScRNAseq mapping asexual life-cycle progression of P.berghei ANKA parasitised RBCs in vivo with and without systemic host inflammation
Ontology highlight
ABSTRACT:
INSTRUMENT(S): NextSeq 550
ORGANISM(S): Mus musculus
SUBMITTER: Hyun Jae Lee
PROVIDER: E-MTAB-12954 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Mucosal-Associated Invariant T (MAIT) cells are an innate-like subset of alpha/beta-T cells expressing semi-invariant TCRs that recognize conserved vitamin B2 metabolite-based antigens from microbes, thus contributing to protection against several bacterial pathogens. To investigate the transcriptomic changes induced during systemic Francisella tularensis infection, liver MAIT cells were recovered from naïve mice and mice at days 13 and 48 post infection.
2021-05-19 | E-MTAB-10239 | biostudies-arrayexpress
Project description:Toal 13 patient samples (Iliac or pyramidal cancellous) were collected with lung cancer who were pathologically diagnosed in Dazhou Central Hospital from June 2020 to January 2021. Patients were monitored by a professional orthopaedic surgeon in the interventional room prior to collecting the samples. This study was approved by the ethics committee and informed consent of patients (IRB2020023). The obtained samples are quickly placed into an Eppendorf tube with PBS buffer for flushing the blood. Then, the samples were cleaned in a cell preservation solution. Finally, the cleaned samples were placed into a sterile EP tube with 2 mL cell preservation solution before being stored in a refrigerator at 4 ° C. Further, the samples with two replicates were sequenced in a 10x genomic chromium platform with a chemistry library (Single Cell 3; v3). The samples were sequenced at BGI (https://www.bgi.com).
2022-11-27 | E-MTAB-11560 | biostudies-arrayexpress
Project description:Plasmodium-specific CD4+ T cells from mice infected with Plasmodium chabaudi chabaudi AS parasites were recovered at Days 0, 7, and 28 to undergo processing and generate scRNA-seq dataset. At Day 28, mice were administered with either saline or artesunate (intermittent artesunate therapy - IAT). scRNA-seq dataset was analysed to investigate transcriptome dynamics of CD4+ T cells from effector to memory states.
2020-10-14 | E-MTAB-9317 | biostudies-arrayexpress
Project description:scRNA-seq was performed and data generated to examine the transcriptomic differences between PD-1/CTLA4 double-positive and double-negative CD4+ T cells in HIV patients.
2022-08-24 | E-MTAB-12039 | biostudies-arrayexpress
Project description:We characterized the proteomic composition of RBCs from 53 breast cancer patients (stages I-III and IV), compared with 33 healthy donors. For that, we performed two different proteomic analyses (LC-MS/MS in DDA mode-shotgun- and a SWATH-MS) using the Triple TOF 6600 technology.
2023-01-17 | PXD030936 | Pride
Project description:Malaria infection triggers vigorous host immune responses; however, the parasite ligands, host receptors and the signaling pathways responsible for these reactions remain unknown or controversial. Malaria parasites primarily reside within red blood cells (RBCs), thereby hiding themselves from direct contact and recognition by host immune cells. Host responses to malaria infection are very different from those elicited by bacterial and viral infections and the host receptors recognizing parasite ligands have been elusive. Here we investigated mouse genome-wide transcriptional responses to infections with two strains of Plasmodium yoelii (N67 and N67C) and discovered differences in innate response pathways corresponding to strain-specific disease phenotypes. Using in vitro RNAi gene knockdown and knockout mice, we demonstrated that a strong IFN-I response triggered by RNA Polymerase III and melanoma differentiation-associated protein 5 (MDA5), not Toll-like receptors (TLRs), binding of parasite DNA/RNA contributed to a decline of parasitemia in N67-infected mice. We showed that conventional dendritic cells were the major sources of early IFN-I, and that surface expression of phosphatidylserine (PS) on infected RBC (iRBC) might promote their phagocytic uptake, leading to the release of parasite ligands and the IFN-I response in N67 infection. In contrast, an elevated inflammatory response mediated by CD14/TLR and p38 signaling played a role in disease severity and early host death in N67C-infected mice. In addition to identifying cytosolic DNA/RNA sensors and signaling pathways previously unrecognized in malaria infection, our study demonstrates the importance of parasite genetic backgrounds in malaria pathology and provides important information for studying human malaria pathogenesis. Spleen RNA from mice, 4 days post infection with Plasmodium yoelii (strain N67 or N67C), or mock infection (N). Replicates from 6 individual mice per condition.
2014-01-13 | E-GEOD-51329 | biostudies-arrayexpress
Project description:The malaria parasite Plasmodium replicates and differentiates in red blood cells of its host. The erythropoietic niches (spleen and bone marrow) are important but poorly understood reservoirs of asexual replication and sexual development. We aimed to understand how the parasite adapts to its host organ and a host cell level. For this, we performed single-cell RNA-seq (scRNA-seq) analysis on host and parasite cells derived from spleen, blood and bone marrow. Organs were harvested from two infected and one uninfected mice and parasite cells were enriched to about 50% by flow sorting (infected samples only). To identify host cells by surface expression (CITE-seq), cells were stained with barcoded antibodies targeting CD44 and CD71. Droplet-based scRNA-seq of these samples was performed using 10X genomics technology and cDNA was sequenced on Illumina.
2021-11-30 | E-MTAB-10800 | biostudies-arrayexpress
Project description:Clonal hematopoiesis of indeterminate potential (CHIP) is caused by somatic mutations in hematopoietic stem cells and is associated with worse prognosis in heart failure patients. Patients harboring CHIP mutations show enhanced inflammation. However, whether these signatures are derived from the relatively low number of cells harboring mutations or are indicators of a systemic pro-inflammatory activation that is associated with CHIP is unclear. In this study, we assessed the cell-intrinsic effects of CHIP mutant-carrying cells in patients with heart failure. Using an improved protocol to detect mutant cells on a single cell level (MutDetect-Seq), we show that DNMT3A mutant monocytes exhibit altered gene expression profiles associated with inflammation and phagolysosome function. Gene expression was also significantly altered in DNMT3A mutant CD4+ T cells and NK cells, but not CD8 T cells. DNMT3A silenced CD4+ T cells and NK cells showed increased effector functions. Moreover, increased paracrine signaling pathways are predicted and validated between mutated and wild monocytes and T cells, which amplify inflammatory circuits. Taken together, these data provide novel insights into how CHIP might promote worse prognosis in heart failure patients.
2023-06-15 | E-MTAB-13016 | biostudies-arrayexpress
Project description:We have used cDNA microarrays to compare gene expression profiles in brains from normal mice to those infected with the Anka strain of Plasmodium berghei, a model of cerebral malaria. For each of three brains in each group, we computed ratios of all quantifiable genes with a composite reference sample and then computed ratios of gene expression in infected brains with untreated controls. Of the almost 12,000 unigenes adequateluy quantified in all arrays, about 3% were significantly downregulated (p<0.05, >50% fold change) and about 7% were upregulated. Upon inspection of the lists of regulated genes, we identified a high number encoding proteins of importance to normal brain function or associated with neuropathology. These results emphasize the important impact of malarial infection on gene expression in brain and provide tentative target biomarkers that might provide novel therapeutic targets for neurological sequelae of disease. We have used a previously published protocol (Iacobas et al., Physiol Genomics 2005) and a composite reference RNA sample (R) prepared in sufficient quantity for the entire experiment from ten adult mouse tissues (aorta, brain, heart, kidney, liver, lung, ovary/testicles, spleen, and stomach - equal amounts from males and females). This combination of source tissues provided a high diversity of genes expressed in the midrange of the detection system for the AECOM mouse cDNA microarrays. Briefly, 60μg total RNA, extracted in Trizol® (Invitrogen, Carlsbad, CA) from brains of three infected (I) and three control (C) mice, purified with RNeasy® mini kit (Qiagen, Valencia, CA), were reverse transcribed into cDNA incorporating fluorescent Cy3-dUTP. The composite reference was reverse transcribed to incorporate Cy5-dUTP. Each of the six Cy3-labeled brain extracts was co-hybridized overnight at 50°C against the Cy5-labeled reference with AECOM 32k Mouse oligonucleotide arrays, MO3 printing series (platform described in http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GPL5371). After hybridization, the slides were washed at room temperature, using solutions containing 0.1% sodium dodecyl sulfate (SDS) and 1% SSC (3M NaCl + 0.3M sodium citrate) to remove the non-hybridized cDNAs.
2010-09-16 | E-GEOD-24086 | biostudies-arrayexpress
Project description:In this study, we investigated somatic mutations in T cells in patients with various hematological disorders. To analyze immune cell phenotypes with somatic mutations, we performed scRNA+TCRab sequencing from 9 patients with chronic GVHD and clonal expansions of CD4+ or CD8+ T cells based on T cell receptor sequencing. CD45+ PBMCs (lymphocytes and monocytes) were sorted with BD Influx cell sorter and subjected to sequencing with Chromium VDJ and Gene Expression platform (v1.1, 10X Genomics). Sequencing was performed with Novaseq 6000 (Illumina). The immune cell phenotypes were compared to healthy controls processed in the same laboratory (accession number E-MTAB-11170). Due to data privacy concerns, the raw sequencing data is in the European Genome-Phenome Archive (EGA) under accession code [xxxx] and can be requested through the EGA Data Access Committee.
2024-04-10 | E-MTAB-13419 | biostudies-arrayexpress