Eimeria falciformis strain:Bayer Haberkorn 1970
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA232109 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR1055960.fastq.gz | Fastqsanger.gz | |||
| SRR1055956_1.fastq.gz | Fastqsanger.gz | |||
| SRR1055956_2.fastq.gz | Fastqsanger.gz |
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Project description:Intracellular parasites reprogram the host functions for their survival and reproduction. Conversely, the infected host attempts to defend the microbial insult. The extent and relevance of parasite-mediated host response in vivo remains poorly studied. We utilized Eimeria falciformis, an obligate intracellular parasite completing its entire life cycle in the mouse intestinal epithelium, to identify and validate the host determinants of the parasite infection. The most prominent mouse genes induced during the onset of asexual (24 hrs) and sexual (144 hrs) parasite cycle include IFNg-regulated factors, e.g., immunity-related GTPases IRGA6/B6/D/M2/M3, guanylate-binding proteins GBP2/3/5/8, chemokines CxCL9-11 and several enzymes of the kynurenine pathway including indoleamine 2,3-dioxygenase 1 (IDO1). These results indicated a multifarious innate defense (tryptophan catabolism, IRG, GBP, chemokines signaling) mounted by epithelial cells, and a consequential adaptive immune response (chemokines-cytokines signaling, lymphocyte recruitment). A notable increase in the inflammation- and immunity-associated transcripts correlated with the severity of infection and influx of B-cells, T-cells and macrophages to the parasitized tissue. Indeed, parasite growth was enhanced in the animals inhibited for CxCr3, a major chemokine receptor on immune cells. Interestingly, despite a prominent induction, the mouse IRGB6 failed to recognize and disrupt the parasitophorous vacuole in the parasite cultures, implying an immune evasion by E. falciformis. Likewise, the oocyst output was impaired in IFNg-R-/- and IDO1-/- mice, which signifies a subversion of IFNg-signaling by the parasite to promote its growth. In brief, the Eimeria-rodent model shows contrasting roles of IFNg-signaling for parasite development, identifies a retinue of potential host determinants, and epitomizes its efficacy for in vivo parasite-host interaction studies. Microarray experiments were performed as dual-color hybridizations on Agilent mouse whole genome catalog 44K arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.
2014-01-01 | E-GEOD-49948 | biostudies-arrayexpress
Project description:Eimeria tenella strain:Guelph Genome sequencing
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Project description:Intraspecific phenotypic variation markedly influences the damage that parasites inflict on their hosts. Such is the case for strains of Eimeria maxima, a costly enteric parasite of poultry, where strain APU-1 exhibits greater pathogenicity than APU-2. Here, we examined how these strains differ as oocysts mature to the fully-sporulated stage. We performed mi-croscopy and RNA-Sequencing on oocysts at regular intervals (6-12 hours) during sporulation. Although each strain underwent parallel development, APU-1 initially approached maturation more slowly. Each strain achieved full sporu-lation and similar transcription profiles by hour 36, after which strains appeared to diverge. These differences may in-fluence subsequent virulence. Candidate biomarkers of oocyst viability include 58 genes contributing at least 1,000 Transcripts Per Million throughout sporulation. Many genes resemble constitutively expressed genes also important to Eimeria acervulina. Mature and immature oocysts differentially express certain genes. Expression of some such bi-omarkers appears strain-specific. These data illuminate processes that may generally underlie sporulation in Eimeria and related genera, such as Cyclospora, and identify biological processes which differentiate among them. Drivers of devel-opment and senescence may provide tools to assess the viability of oocysts, which would greatly benefit the poultry industry and food safety applications.
2024-01-31 | GSE247034 | GEO
Project description:Eimeria acervulina Genome sequencing and assembly
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Project description:Successful asexual reproduction of intracellular pathogens depend on their potential to exploit host resources and subvert antimicrobial defense. Here, we deployed two prevalent intracellular parasites of mammalian cells, namely Toxoplasma gondii and Eimeria falciformis, to identify the potential host determinants of infection. Expression analyses of the young adult mouse colonic (YAMC) epithelial cells showed regulation of several distinct transcripts upon infection by either parasite, indicating that closely-related pathogens program their intracellular niches in notably adaptive manner. Conversely, parasitized mouse embryonic fibroblasts (MEFs) exhibited a divergent transcriptome compared to corresponding YAMC cells, suggesting that individual host cells mount fairly discrete response while encountering a given pathogen. Among a limited set of factors similarly regulated by both parasites, we identified cFos, a master transcription factor, that was consistently induced throughout infection. Indeed, the asexual development of T. gondii and E. falciformis was severely impaired in MEF cells lacking cFos expression. Last but not least, our comparative transcriptomics of the parasitized MEFs (wild-type and cFos-/- mutant) and YAMC epithelial cells disclosed a cFos-network, underlying signal transduction cascades, as well as a repertoire of nucleotides-binding and ion-binding proteins, which are likely co-opted by coccidian pathogens to acclimatize the mammalian host environment.
2021-01-27 | GSE157395 | GEO
Project description:Intracellular parasites reprogram the host functions for their survival and reproduction. Conversely, the infected host attempts to defend the microbial insult. The extent and relevance of parasite-mediated host response in vivo remains poorly studied. We utilized Eimeria falciformis, an obligate intracellular parasite completing its entire life cycle in the mouse intestinal epithelium, to identify and validate the host determinants of the parasite infection. The most prominent mouse genes induced during the onset of asexual (24 hrs) and sexual (144 hrs) parasite cycle include IFNg-regulated factors, e.g., immunity-related GTPases IRGA6/B6/D/M2/M3, guanylate-binding proteins GBP2/3/5/8, chemokines CxCL9-11 and several enzymes of the kynurenine pathway including indoleamine 2,3-dioxygenase 1 (IDO1). These results indicated a multifarious innate defense (tryptophan catabolism, IRG, GBP, chemokines signaling) mounted by epithelial cells, and a consequential adaptive immune response (chemokines-cytokines signaling, lymphocyte recruitment). A notable increase in the inflammation- and immunity-associated transcripts correlated with the severity of infection and influx of B-cells, T-cells and macrophages to the parasitized tissue. Indeed, parasite growth was enhanced in the animals inhibited for CxCr3, a major chemokine receptor on immune cells. Interestingly, despite a prominent induction, the mouse IRGB6 failed to recognize and disrupt the parasitophorous vacuole in the parasite cultures, implying an immune evasion by E. falciformis. Likewise, the oocyst output was impaired in IFNg-R-/- and IDO1-/- mice, which signifies a subversion of IFNg-signaling by the parasite to promote its growth. In brief, the Eimeria-rodent model shows contrasting roles of IFNg-signaling for parasite development, identifies a retinue of potential host determinants, and epitomizes its efficacy for in vivo parasite-host interaction studies.
2014-01-01 | GSE49948 | GEO
Project description:Eimeria are obligate intracellular protozoan parasites which can affect chickens. After exposure to Eimeria chickens establish (partial) protective immunity to the homologues strain. In this paper we investigate the process responsible for Eimeria protection. In order to find host reactions specificly involved in protection to homologous re-infection we investigated the host reactions after primary infection and a homologous or heterologous secondary infection.<br><br>Broilers were mock infected or infected with E.maxima (Max) at one week of age. Two weeks later broilers were mock infected, infected with E.maxima or E.acervulina. Oocyst output, T-cell population and cytokine mRNA expression profiles and Eimeria DNA profiles were measured 2, 4 and 7 days pi. Specific regulation of gene expression profiles was monitored by a whole genome oligo-array containing 20.673 oligoï¾´s at 8 and 24 hours pi.<br><br>
2009-08-01 | E-MEXP-1972 | biostudies-arrayexpress
Project description:In order to elucidate the infection mechanisms of Eimeria tenella and the chicken immune response, chickens were infected with Eimeria tenella strain Hougton sporozoites. Samples were taken at 0, 1, 2, 3, 4 and 10 days post-infection and mRNA sequenced. A dual-RNA seq analysis was carried out, comparing the expression of infected chickens during each sampling time point with uninfected chickens and comparing E. tenella samples during the infection with a sample of pure sporozoites. The results show a variety of response signals in the chicken, both previously known and unknown, as well as a clear role for a variety of infection-related genes in E. tenella
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