Ontology highlight
ABSTRACT:
PROVIDER: PRJNA278775 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3124390.fastq.gz | Fastqsanger.gz | |||
| SRR3124390_1.fastq.gz | Fastqsanger.gz | |||
| SRR3124390_2.fastq.gz | Fastqsanger.gz | |||
| SRR3124391.fastq.gz | Fastqsanger.gz | |||
| SRR3124391_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 9 |
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Project description:The sexually transmitted parasite Trichomonas vaginalis is often found in symbiosis with the obligate intracellular pathogen Mycoplasma hominis. M. hominis is itself an opportunistic pathogen of the female reproductive tract associated with bacterial vaginosis. The goal of this experiment was to identify the effects of each pathogen individually and in symbiosis on host cell gene expression.
2024-10-03 | GSE278319 | GEO
Project description:Microsporidia are single-celled intracellular parasites that cause opportunistic diseases in humans. Encephalitozoon intestinalis is a prevalent human-infecting species that invades the small intestine. Dissemination to other organ systems is also observed, and is potentially facilitated by macrophages. The macrophage response to infection and the developmental trajectory of the parasite are not well studied. Here we use single cell RNA sequencing to investigate transcriptional changes in both the host and parasite during infection. While a small population of infected macrophages mount a response, most remain transcriptionally unchanged, suggesting that the majority of parasites may avoid host detection. The parasite transcriptome reveals large transcriptional changes throughout the life cycle, providing a blueprint for parasite development. The stealthy microsporidian lifestyle likely allows these parasites to harness macrophages for replication and dissemination. Together, our data provide insights into the host response in primary human macrophages and the E. intestinalis developmental program.
2024-06-26 | GSE268707 | GEO
Project description:The purpose of this study is the investigation of new host-microbiome interactions promoting adenoma formation and adenocarcinoma progression. For that purpose, the investigators will collect saliva, stool and colon biopsy specimens from patients referred to colonoscopy or surgical resection of colorectal tumor. Besides, a questionnaire about diet, lifestyle and medical history will be collected. Sample analysis will involve simultaneous characterization of host and microbiota genomic and transcriptomic components.
| 2228596 | ecrin-mdr-crc
Project description:Vanee2010 - Genome-scale metabolic model of
Cryptosporidium hominis (iNV213)
This model is described in the article:
A genome-scale metabolic
model of Cryptosporidium hominis.
Vanee N, Roberts SB, Fong SS, Manque
P, Buck GA.
Chem. Biodivers. 2010 May; 7(5):
1026-1039
Abstract:
The apicomplexan Cryptosporidium is a protozoan parasite of
humans and other mammals. Cryptosporidium species cause acute
gastroenteritis and diarrheal disease in healthy humans and
animals, and cause life-threatening infection in
immunocompromised individuals such as people with AIDS. The
parasite has a one-host life cycle and commonly invades
intestinal epithelial cells. The current genome annotation of
C. hominis, the most serious human pathogen, predicts 3884
genes of which ca. 1581 have predicted functional annotations.
Using a combination of bioinformatics analysis, biochemical
evidence, and high-throughput data, we have constructed a
genome-scale metabolic model of C. hominis. The model is
comprised of 213 gene-associated enzymes involved in 540
reactions among the major metabolic pathways and provides a
link between the genotype and the phenotype of the organism,
making it possible to study and predict behavior based upon
genome content. This model was also used to analyze the two
life stages of the parasite by integrating the stage-specific
proteomic data for oocyst and sporozoite stages. Overall, this
model provides a computational framework to systematically
study and analyze various functional behaviors of C. hominis
with respect to its life cycle and pathogenicity.
This model is hosted on
BioModels Database
and identified by:
MODEL1507180071.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2015-07-30 | MODEL1507180071 | BioModels
Project description:We developed a stem cell-derived culture system for C. hominis using human enterocytes differentiated under air-liquid interface (ALI) conditions. Human ALI (hALI) cultures supported robust growth and complete development of C. hominis in vitro including all life cycle stages. C. hominis infection induced a strong interferon response from enterocytes, likely driven by an endogenous dsRNA virus in the parasite. Prior infection with Cryptosporidium induced type III IFN secretion and consequently blunted infection with Rotavirus, suggesting such co-infections may alter vaccine efficacy.
2023-10-02 | GSE241571 | GEO
Project description:We developed a stem cell-derived culture system for C. hominis using human enterocytes differentiated under air-liquid interface (ALI) conditions. Human ALI (hALI) cultures supported robust growth and complete development of C. hominis in vitro including all life cycle stages. C. hominis infection induced a strong interferon response from enterocytes, likely driven by an endogenous dsRNA virus in the parasite. Prior infection with Cryptosporidium induced type III IFN secretion and consequently blunted infection with Rotavirus, suggesting such co-infections may alter vaccine efficacy.
2023-10-02 | GSE241570 | GEO
Project description:M. hominis adherence, colonisation and invasion of HeLa cells were characterised in a time-course study using microarray-based analysis of the HeLa cell transcriptome: 0 h to monitor the baseline of transcription, 4 h to examine host reactions to mycoplasma attachment, 48 h to capture in addition the initiation of invasion, and 2 weeks post infection to examine a chronically infected host cell. At 4 h post infection, cytoadherence of M. hominis to the HeLa cell surface was accompanied by differential regulation of 723 host genes (>2 fold change in expression). Genes associated with immune responses and signal transduction pathways were mainly affected and components involved in cell-cycle regulation, growth and death were highly upregulated. At 48 h post infection, when mycoplasma invasion started, 1588 host genes were differentially expressed and expression of genes for lysosome-specific proteins associated with bacterial lysis was detected. In a chronically infected HeLa cell line (2 weeks), of the 1972 regulated host genes, components of the ECM-receptor interaction pathway and phagosome-related integrins were markedly increased. The immune response was quite different to that at the beginning of infection, with a prominent induction of IL1B gene expression, affecting pathways of MAPK signalling, and genes connected with cytokine-cytokine interactions and apoptosis. These data show for the first time the complex, time-dependent reaction of the host directed at mycoplasmal clearance and the counter measures of this pestering pathogen. To elucidate the host-reactions at the different stages of M. hominis infection, four time points post infection (0h, 4h, 48h, 2 weeks) were chosen for microarray gene expression analyses. Total RNA was prepared from infection assays (MOI 100) in parallel with uninfected HeLa cells and the host cell transcriptomes were determined by comparative microarray analyses.
2014-02-06 | E-GEOD-54698 | biostudies-arrayexpress
Project description:Microsporidia are intracellular eukaryotic pathogens that pose a substantial threat to immunocompromised hosts. The way these pathogens manipulate host cells during infection remains poorly understood. Using a proximity biotinylation strategy we established that microsporidian EnP1 is a nucleus-targeted effector that modifies the host cell environment. EnP1's translocation to the host nucleus is meditated by nuclear localization signals (NLSs). In the nucleus, EnP1 interacts with host histone H2B. This interaction disrupts H2B monoubiquitination (H2Bub), subsequently impacting p53 expression. Crucially, this inhibition of p53 weakens its control over the downstream target gene SLC7A11, enhancing the host cell's resilience against ferroptosis during microsporidian infection. This favorable condition promotes the proliferation of microsporidia within the host cell. These findings shed light on the molecular mechanisms by which microsporidia modify their host cells to facilitate their survival.
2023-11-21 | GSE247835 | GEO
Project description:Mycoplasma hominis (M. hominis) belongs to the class Mollicutes, characterized by a very small genome size, metabolic pathway reduction, including transcription factors, and the absence of a cell wall. Despite this, they adapt well not only to specific niches within the host organism but can also spread throughout the body, colonizing various organs and tissues. The mechanisms of adaptation in M. hominis, as well as the pathways regulating them, are poorly understood. It is known that when adapting to adverse conditions, mycoplasmas can undergo phenotypic switches that may persist for several generations. To investigate the adaptive properties of M. hominis associated with survival in the host organism, we conducted a comparative proteogenomic analysis of 8 clinical isolates of M. hominis obtained from patients with urogenital infections, along with the laboratory strain H-34.
2024-06-22 | PXD048835 | Pride
Project description:Microsporidian parasite causing keratoconjunctivitis in immunosuppressed patients
| PRJNA53983 | ENA