Ontology highlight
ABSTRACT:
PROVIDER: PRJNA595895 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10695800.fastq.gz | Fastqsanger.gz | |||
| SRR10695801.fastq.gz | Fastqsanger.gz | |||
| SRR10695802.fastq.gz | Fastqsanger.gz | |||
| SRR10695803.fastq.gz | Fastqsanger.gz | |||
| SRR10695804.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 56 |
Similar Datasets
Project description:Expression profiling of Sudanese visceral leishmaniasis patients pre- and post-treatment with sodium stibogluconate
| PRJNA377721 | ENA
Project description:Visceral leishmaniasis (VL) in Sudan caused by Leishmania donovani is fatal in susceptible individuals if untreated. Treatment with Sodium Stibogluconate (SSG) leads to post kala azar dermal leishmaniasis (PKDL) in 58% of patients. Here Affymetrix microarrays were used to identify genes differentially expressed in lymph nodes (N=9 paired samples) pre- and post-treatment with SSG. Using the Bioconductor package limma, 438 genes from 28,869 post quality-control probe-sets were differentially expressed (Pnominal≤0.02) post- versus pre-treatment. Canonical pathway analysis using Ingenuity Pathway Analysis identified “Role of NFAT in Regulation of Immune Response” (Pnominal=1.35x10-5; PBH-adjusted=4.79x10-3), “B Cell Development” (Pnominal=2.04x10-4; PBH-adjusted=0.024), “Fcγ Receptor-mediated Phagocytosis in Macrophages and Monocytes” (Pnominal=2.04x10-4; PBH-adjusted=0.024), and “OX40 Signaling” (Pnominal=2.82x10-4; PBH-adjusted=0.025) as pathways differentially regulated post- versus pre-treatment. Major network hub genes included TP53, FN1, MYC, BCL2, JUN, SYK, RUNX2, MMP1 and ACTA2. Top endogenous upstream regulators included IL-7 (P=2.28x10-6), TNF (P=4.26x10-6), APP (P=4.23x10-5) and SPI1/PI.1 (P=1.17x10-7). Top predicted chemical drug regulators included the flavonoid genistein (P=4.56x10-7) and the quinoline alkaloid camptothecin (P=5.14x10-5). These results contribute to our understanding of immuno-pathology associated with VL and response to SSG treatment. Further replication could identify novel therapeutic strategies that improve on SSG treatment and reduce the likelihood of progression to PKDL.
2017-03-03 | GSE95625 | GEO
Project description:Leishmaniasis affects mainly the poorest population of the third world. Among visceral and cutaneous leishmaniasis (VL and CL, respectively), visceral leishmaniasis is the deadliest parasitic disease. There are no vaccines against leishmaniasis and the chemotherapeutic agents currently used are also insufficient. Pentavalent antimonials are being used for the effective treatment of Leishmaniasis. In this study, we characterized compounds with leishmanicidal activity, and determined its mode of action through the whole transcriptome analyiss. The Lesihmania strains were treated with previously identified selected anti-leishmanial compounds in promastigotes cultures on M199 medium (supplemented with L-glutamine, 10% heat-inactivated fetal bovine serum, 0.25% hemin, 40 mM NaHCO3, 100μM adenine, 40 mM HEPES, 100 U/mL penicillin and 100μg/mL streptomycin). Following the total RNA isolation, RNA-seq was performed using the Illumina NextSeq500 system. The genes expression profiling in the treated and control samples were determined using the standard bioinormatics tools, and then compared statistically.
2024-02-01 | GSE239675 | GEO
Project description:Proteomic data relating to: Ontogeny independent expression of LPCAT2 in granuloma macrophages during experimental visceral leishmaniasis
2024-11-21 | MSV000096486 | MassIVE
Project description:RNA-seq transcriptomics of whole blood samples from longitudinal follow-up of a cohort of visceral leishmaniasis (VL) patients with and without HIV coinfection, from active disease through apparent cure and potential relapse. Analysis will identify potential correlates of relapse to identify immune mechanisms underlying the high rate of relapse in HIV/VL coinfection. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ .
| EGAD00001008361 | EGA
Project description:RNA-seq transcriptomics of whole blood samples from longitudinal follow-up of a cohort of visceral leishmaniasis (VL) patients with and without HIV coinfection, from active disease through apparent cure and potential relapse. Analysis will identify potential correlates of relapse to identify immune mechanisms underlying the high rate of relapse in HIV/VL coinfection. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
| EGAS00001003465 | EGA
Project description:Given the discontinuation of various first-line drugs for visceral leishmaniasis (VL), large-scale in vivo drug screening, establishment of a relapse model in rodents, immunophenotyping and transcriptomics were combined to study persistent infections and therapeutic failure. Double bioluminescent/fluorescent Leishmania infantum and L. donovani reporter lines enabled the identification of long-term hematopoietic stem cells (LT-HSC) as a niche with remarkably high parasite burdens, a feature confirmed for human hematopoietic stem cells (hHSPC). LT-HSC are more tolerant to antileishmanial drug action and serve as source of relapse. A unique transcriptional “StemLeish” signature in these cells was defined byupregulated TNF/NF-kB and RGS1/TGF-β/SMAD/SKIL signalling, and a downregulated oxidative burst.Cross-species analyses demonstrated significant overlap with human VL and HIV co-infected blood transcriptomes. In summary, the identification of LT-HSC as a drug- and oxidative stress-resistant niche,undergoing a conserved transcriptional reprogramming underlying Leishmania persistence and treatment failure, may open new therapeutic avenues for leishmaniasis.
2022-06-04 | GSE205452 | GEO
Project description:As a vector-borne disease, leishmaniasis is caused by a parasitic protozoans of leishmania genus and transmitted by female Phlebotomine sandflies. Depending on the body location where immotile form of the parasite namely amastigote is proliferated, three main clinical forms as cutaneous, muco-cutaneous and visceral leishmaniases are defined. While manifestation of cutaneous leishmaniasis is skin lesions on the exposed part of the body, enlarged lymph nodes, spleen or liver along with fever, fatigue and weight loss are the symptoms of visceral leishmaniasis. The most dangerous form is visceral leishmaniasis since it may end up with fatalities if patients are not treated. The purpose of this study was to investigate the difference between the protein expression profiles of leishmania isolates obtained from visceral and cutaneous leishmaniasis patients. To compare two sample groups to each other genetically, L.infantum was chosen since it causes both visceral and cutaneous leishmaniasis. Additionally, another sample group as cutaneous leishmaniasis caused by L.tropica was included to make the comparison both intra- and interspecies level. For protein profiling, both gel-based and gel-free proteomic approaches were carried out. In brief, a total of 15 samples, 5 from each group, were separated on pI 3-10 2D-PAGE gel. Additionally, 9 of those 15 samples, 3 from each group, were analyzed according to qualitative shotgun proteomics method and differential proteins were determined by drawing venn diagram.
2022-01-14 | PXD016333 | Pride
Project description:Transcriptomic and immunopathology analysis on infection of mice with visceral leishmaniasis and a comparison of murine infection compared to hamster
2018-04-20 | GSE113376 | GEO
Project description:Among the most central questions in Leishmania research is why some species remain in the skin dermis at the site of infection by the sand fly vector whereas other species migrate to visceral organs where they cause fatal visceral leishmaniasis. Although L. donovani is the species typically responsible for visceral leishmaniasis, an atypical L. donovani strain is the etiologic agent for cutaneous leishmaniasis in Sri Lanka. To identify molecular determinants for visceral disease, we have analysed the phenotype and genotype of two L. donovani clinical isolates from Sri Lanka where one isolate was derived from a cutaneous leishmaniasis patient (CL) and the other from a visceral leishmaniasis patient (VL). These isolates cause dramatically different pathology when introduced into mice; notably the CL isolate has lost the ability to survive in visceral organs while the VL isolate was highly virulent in visceral organs of BALB/c mice. Whole genome sequencing of the CL and VL isolates revealed that these genomes were very similar as there were no gene deletions and few individual gene amplifications. Indels resulting in frame shifts and loss/gain of stop codons resulted in 13 distinct pseudogenes present in each of the CL and VL isolates. There were 154 non-synonymous SNPs specific to the CL isolate and 193 non-synonymous SNPs specific to the VL isolate. Genome wide gene expression analysis revealed several transcript level differences, including the A2 virulence gene resulting in higher expression of A2 proteins in the VL isolate than in the CL isolate. Genotypic variations relevant to pathology and tropism in Leishmania can be interrogated by reverse genetics. Experimentally increasing A2 expression in the CL isolate through gene transfer significantly increased itM-bM-^@M-^Ys ability to survive in the spleen of BALB/c mice and conversely, down-regulating A2 expression in the VL isolate abrogated attenuated its survival in BALB/c mice. These observations reveal that there are relatively few genetic differences between the CL and VL isolates apart from the A2 genes, but collectively these have profound effects on human disease and experimentally infected mice. 6 Samples in total, 3 each from VL and CL causing isolates were analyzed by Splice Leader RNASeq. These three samples from each of the isolates were grown to form one of the following three lifestages, Promastigotes, Macrophage derived Amastigotes, Axenic Amastigotes.
2013-12-31 | E-GEOD-48475 | biostudies-arrayexpress