Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1013320 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25928144_1.fastq.gz | Fastqsanger.gz | |||
| SRR25928144_2.fastq.gz | Fastqsanger.gz | |||
| SRR25928145_1.fastq.gz | Fastqsanger.gz | |||
| SRR25928145_2.fastq.gz | Fastqsanger.gz | |||
| SRR25928146_1.fastq.gz | Fastqsanger.gz |
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Project description:Cryptosporidium parvum is an important zoonotic parasitic disease worldwide, but the molecular mechanisms of the host–parasite interaction are not fully understood. Noncoding microRNAs (miRNAs) are considered key regulators of parasitic diseases. Therefore, we used microarray, qPCR, and bioinformatic analyses to investigate the intestinal epithelial miRNA expression profile after Cryptosporidium parvum infection.Twenty miRNAs were differentially expressed after infection (four upregulated and 16 downregulated). Further analysis of the differentially expressed miRNAs revealed that many important cellular responses were triggered by Cryptosporidium parvum infection, including cell apoptosis and the inflammatory and immune responses.This study demonstrates for the first time that the miRNA expression profile of human intestinal epithelium cells is altered by C. parvum infection. This dysregulation of miRNA expression may contribute to the regulation of host biological processes in response to C. parvum infection, including cell apoptosis and the immune responses. These results provide new insight into the regulatory mechanisms of host miRNAs during cryptosporidiosis, which may offer potential targets for future C. parvum control strategies.
2018-12-23 | GSE95365 | GEO
Project description:Cryptosporidium is a protozoan parasite that infects the gastrointestinal tract of humans and animals. It is an important opportunistic pathogen in children under the age of two and immunocompromised adults. There is currently no fully effective therapy or vaccine. Long noncoding RNAs are RNA transcripts, over 200 nt in length, that are capable of regulating gene expression through both transcriptional and translational methods. Our lab previously identified a panel of host long noncoding RNAs are that upregulated during Cryptosporidium infection, including NR_033483. Further experiments indicated this host long noncoding RNA may be playing a pro-parasitic role during infection. We hypothesized that NR_033483 is regulating the expression of host immune genes to aid the parasite. In this study, we treated intestinal epithelial cells with an siRNA targeting NR_033483 to knockdown its expression, or a scrambled siRNA control, and infected the samples with Cryptosporidium. We sought to determine changes in host gene expression when NR_033483 was knocked down verse control samples.
2023-05-31 | E-MTAB-12972 | biostudies-arrayexpress
Project description:Cryptosporidium is a leading cause of severe diarrhea and diarrheal-related death in children worldwide. As an obligate intracellular parasite, Cryptosporidium relies on intestinal epithelial cells to provide a niche for its growth and survival, but little is known about the contributions that the infected cell makes to this relationship. Here we conducted a genome wide CRISPR/Cas9 knockout screen to discover host genes required for Cryptosporidium parvum infection and/or host cell survival. The gene enrichment analysis indicated that the host interferon response, glycosaminoglycan (GAG) and glycosylphosphatidylinositol (GPI) anchor biosynthesis are important determinants of susceptibility to C. parvum infection. Several of these pathways are linked to parasite attachment and invasion and C-type lectins on the surface of the parasite. Evaluation of transcript and protein induction of innate interferons revealed a pronounced type III interferon response to Cryptosporidium in human cells as well as in mice. Treatment of mice with IFNλ reduced infection burden and protected immunocompromised mice from severe outcomes including death, with effects that STAT1 signaling in the enterocyte. Initiation of this type III interferon response was dependent on sustained intracellular growth and mediated by the pattern recognition receptor TLR3. We conclude that host cell intrinsic recognition of Cryptosporidium results in IFNλ production critical to early protection against this infection.
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Project description:Cryptosporidium infects enterocytes, but their contribution to parasite control is not well understood. Early resistance to Cryptosporidium is dependent on the production of IFN gamma. Loss of STAT1 in enterocytes, but not dendritic cells or macrophages, antagonized early parasite control. Moreover, transcriptional profiling of enterocytes from infected mice revealed the induction of an IFN gamma signature that included multiple genes (IDO, GBP, IRG) associated with control of intracellular pathogens.
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Project description:Cryptosporidiosis is a zoonotic disease caused by infection with the oocyst of Cryptosporidium in human and animals. MicroRNA (miRNA) emerges as important player in regulating the innate immune response against parasitic infection. Here, we compared miRNA profiles of the glandular stomach of Cryptosporidium muris (C. muris) infected and un-infected BALB/c mice using microarray sequencing. A total of 10 miRNAs (including 3 upregulated and 7 downregulated miRNAs) with significant expression differences (|FC| ≥ 2 and P value test < 0.05) were screened after C. muris infected the glandular stomach of BALB/c mice for 8 hours. MiRWalk and miRDB online bioinformatics software were used to predict the target genes of differentially expressed miRNAs. Gene Ontology (GO) and KEGG enrichment analyses were performed for annotate the target genes. GO terms indicates that many are associated with the relevant generic transcription and ion transport. In addition, the KEGG analyses showed that the target genes were strictly related to a diverse types of tumor disease progression and the antipathogen immunity pathway. In the current study, we first reported the changes of miRNA expression profile in glandular stomach of BALB/c mice at the early phase of C. muris invasion. As such, dysregulation of miRNA expression profile may contribute to our understanding of the Cryptosporidiosis pathology. The result reported in this paper provide a new perspective into the miRNA regulatory mechanisms of Cryptosporidiosis, which may help to develop effective control strategies against Cryptosporidium.
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Project description:H69 cells were cultured in H69 medium with Cryptosporidium parvum oocysts(10 X 5 per well, for smaples 04, 05 and 06) or without oocysts(for samples 01, 02 and 03)for 8 hours and then collected for array analysis. Sample 07 was cells exposed to heated inactived oocysts. <br>
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