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Transcriptomic analysis of Plasmodium PBANKA, PBSLTRiP-KO, PB268-KO parasite infected and uninfected host cell

ABSTRACT: Liver stage of malaria parasite exports SLTRiP and PB268 to the cytosol of parasite infected host cell. To know the host genes perturbed by WT-PBANKA, SLTRiP-KO and PB268-KO parasite growth, we did transcriptomic sequencing of infected host cells. We did mRNA sequencing of four samples for comparative analysis of WT and PB-knockout parasites infected host cells at 22 hours of post sporozoites infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53292 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA231615

REPOSITORIES: GEO

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Transcriptomic analysis of Plasmodium PBANKA, PBSLTRiP-KO, PB268-KO parasite infected and uninfected host cell

Project description:Liver stage of malaria parasite exports SLTRiP and PB268 to the cytosol of parasite infected host cell. To know the host genes perturbed by WT-PBANKA, SLTRiP-KO and PB268-KO parasite growth, we did transcriptomic sequencing of infected host cells. We did mRNA sequencing of four samples for comparative analysis of WT and PB-knockout parasites infected host cells at 22 hours of post sporozoites infection. mRNA profiles of Plasmodium PBANKA, PBSLTRiP-KO, PB268-KO parasite infected and uninfected HepG2 cells after 22hrs of sporozoites infections were generated by deep sequencing using Illumina GAIIx.

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Comparison of gene expression between wild type and AP2-G KO parasites.

Project description:In the rodent malaria parasite Plasmodium berghei, we found that an AP2 family transcription factor designated AP2-L plays a critical role in the development of the liver stage. Using DNA microarray analysis we showed that the expression of several genes, including those of parasitophorous vacuole membrane proteins, was significantly decreased in the early liver stage of AP2-L-depleted parasites. Gene expression of P. berghei sporozoites was compared between wild type and AP2-G KO parasites. Five biologically independent experiments were performed for each genotype.

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ATAC-seq Identification of Chromatin Accessibility in Both Human Host Cells and the Parasite Toxoplasma gondii

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Host cell transcripts during malaria liver stage infection reveals a coordinated and sequential set of biological events

Project description:After entering their mammalian host via the bite of an Anopheles mosquito, Plasmodium sporozoites migrate to the liver where they traverse several hepatocytes before invading the one inside which they will develop and multiply into thousands of merozoites. Although this constitutes an essential step in malaria infection, the requirements of Plasmodium parasites in liver cells and how they use the host cell for their own survival and development are poorly understood. To gain new insights into the molecular host-parasite interactions that take place during malaria liver infection, we have used high-throughput microarray technology to determine the transcriptional profile of P. yoelii-infected hepatocytes that were collected from P. yoelii-infected mice 24 and 40 h after infection. This in vivo microarray expression was compared with the microarray analysis of in vitro infected hepatoma cells infected with closely related rodent malaria parasite P. berghei. Differential expression patterns for host genes identify genes and pathways involved in the host response to rodent Plasmodium parasites. Keywords: gene expression

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Simultaneous host parasite time course analysis of mouse and the whipworm Trichuris muris to identify candidate genes for host parasite interaction

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Project description:During infections with malaria parasites P. vivax, patients exhibit rhythmic fevers every 48 hours. These fever cycles correspond with the time parasites take to traverse the Intraerythrocytic Cycle (IEC) and may be guided by a parasite-intrinsic clock. Different species of Plasmodia have cycle times that are multiples of 24 hours, suggesting they may be coordinated with the host circadian clock. We utilized an ex vivo culture of whole blood from patients infected with P. vivax to examine the dynamics of the host circadian transcriptome and the parasite IEC transcriptome. Transcriptome dynamics revealed that the phases of the host circadian cycle and the parasite IEC were correlated across multiple patients, suggesting that the cycles are coupled. In mouse model systems, host-parasite cycle coupling appears to provide a selective advantage for the parasite. Thus, understanding how host and parasite cycles are coupled in humans could enable anti-malarial therapies that disrupt this coupling.

2023-06-12 | GSE209877 | GEO

Parasite secreted products modulate STAT6-dependent and -independent transcription in macrophages

Project description:Toxoplasma gondii is an obligate intracellular protozoan parasite which, upon invasion of host cells, injects virulence factors that are known to induce dramatic alterations in host cell signaling. Although much work has been directed at understanding the impact of specific secreted proteins on host cell function, dissecting the host response to injected virulence factors has been complicated by the fact that injection is rapidly followed by invasion, establishment of a parasitophorous vacuole in the host cell cytoplasm, secretion of parasite proteins from other specialized organelles, and remodeling of the host cell cytoskeleton Here, we describe the global macrophage transcriptional response to secreted proteins and show that injection of rhoptry contents alone is sufficient to trigger a dramatic host cells response. We further define modules of genes that are regulated in a parasite strain-specific manner by activation of the host transcription factor, STAT6. Our approach leverages transgenic parasites that express mCherry and inject Cre-recombinase along with normal virulence factors into the cytoplasm of host cells. Primary macrophages were recovered from transgenic reporter mice (Ai6) that express the ZsGreen1 fluorochrome when exposed to cre recombinase, allowing for the identification of a unique population of cells into which T. gondii injects virulence factors but does not infect (uninfected-injected, or U-I). Transcriptional profiling of these U-I cells compared to infected cells or uninfected controls from the same cultures was carried out, using bone marrow derived macrophages (BMDM) from either WT or STAT6-/- mice. This data allows us to interrogate the outcomes T. gondii induced STAT signaling in both infected and U-I cell populations, and to resolve effects of injected virulence factors, like ROP16, from those changes induced by infection.

2019-03-01 | GSE55892 | GEO

Simultaneous Host and Parasite Expression Profiling Identifies Transcriptional Programs Associated with Cerebral Malaria

Project description:The development and outcome of cerebral malaria (CM) reflects a complex interplay between parasite-expressed virulence factors and host response to infection. To simultaneously analyze transcriptional programs in both parasite and host over the course of infection, we created microarrays to concurrently detect transcripts in the genomes of both Plasmodium berghei and mouse. Analysis of RNA from brain, lung, liver, and spleen of mice infected with P. berghei ANKA showed that parasite gene expression is readily detected in whole organ RNA. Comparison of CM-susceptible (C57BL/6) and CM-resistant (BALB/c) mice showed that both host and parasite display distinct organ-specific transcriptional signatures in susceptible versus resistant animals. Host genes whose expression differs between CM-resistant and CM-susceptible mice, at either baseline or induced by infection, tend to relate to humoral and immune response, complement activation, or cell-cell interactions, suggesting differences in immune function that may directly underlie protection from or susceptibility to CM. P. berghei, in contrast, displayed differential expression of genes related to apparent biosynthestic activities, with the majority of transcriptional activity observed in the lung. These data show that analysis of host and parasite gene expression profiles by hybridizing infected host samples to a single microarray is feasible, and can facilitate dissection of complex host-pathogen interactions. Keywords: Time course, Disease state analysis

2006-11-24 | GSE5672 | GEO

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