Genome-wide gene expression analysis of WERI-Rb-1 (retinal cells) infected with Toxoplasma gondii over time
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE81016 | GEO | 2016/05/03
SECONDARY ACCESSION(S): PRJNA320290
REPOSITORIES: GEO
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Project description:Analysis of DNA methylation patterns following infection of the parasite Toxoplasma gondii in a clinically relevant retinal cell line over a time course of 2 hours, 6 hours and 24 hours. Parasites were washed off after 2 hours to ensure that methylation changes are truly reflective of an on-going infection, and not on-going parasite invasion.
2016-05-03 | GSE81015 | GEO
Project description:Analysis of host cell gene expression patterns following infection of the parasite Toxoplasma gondii over a time course of 2 hours, 6 hours and 24 hours. Parasites were washed off after 2 hours to ensure that gene expression changes are truly reflective of an on-going infection, and not on-going parasite invasion.
2017-07-05 | GSE98677 | GEO
Project description:The innate immune response of mucosal epithelial cells during pathogen invasion plays a central role in immune regulation in the gut. Toxoplasma gondii (T. gondii) is a protozoan intracellular parasite that is usually transmitted through oral infection. Although much of the information on immunity to T. gondii has come from intra-peritoneal infection models, more recent studies have revealed the importance of studying immunity following infection through the natural per-oral route. Oral infection studies have identified many of the key players in the intestinal response; however, they have relied on responses detected days to weeks following infection. Much less is known about how the gut epithelial layer senses and reacts during initial contact with the pathogen. Given the importance of epithelial cells during pathogen invasion, this study uses an in vitro approach to isolate the key players and examine the early response of intestinal epithelial cells during infection by T. gondii. We show that human intestinal epithelial cells infected with T. gondii elicit rapid MAPK phosphorylation, NF-κB nuclear translocation, and secretion of interleukin (IL)-8. Both ERK1/2 activation and IL-8 secretion responses were shown to be MyD88 dependent and TLR2 was identified to be involved in the recognition of the parasite regardless of the parasite genotype. Furthermore, we were able to identify additional T. gondii-regulated genes in the infected cells using a pathway-focused array. Together, our findings suggest that intestinal epithelial cells were able to recognize T. gondii during infection, and the outcome is important for modulating intestinal immune responses. Oral infection studies have demonstrated an increase in several cytokines and chemokines in response to T.gondii infection; however, the mixed population of the intestinal mucosa did not allow for the determination of the relative role that specific cell populations play in the production of these mediators. To address the role of intestinal epithelial cells to modulate the cytokine environment early following infection, we used specific pathway arrays to identify cytokines and chemokines induced 4 hours after exposure to T. gondii. At this time point most cells have become infected, but the parasites have not replicated.
2010-05-05 | E-GEOD-18085 | biostudies-arrayexpress
Project description:The innate immune response of mucosal epithelial cells during pathogen invasion plays a central role in immune regulation in the gut. Toxoplasma gondii (T. gondii) is a protozoan intracellular parasite that is usually transmitted through oral infection. Although much of the information on immunity to T. gondii has come from intra-peritoneal infection models, more recent studies have revealed the importance of studying immunity following infection through the natural per-oral route. Oral infection studies have identified many of the key players in the intestinal response; however, they have relied on responses detected days to weeks following infection. Much less is known about how the gut epithelial layer senses and reacts during initial contact with the pathogen. Given the importance of epithelial cells during pathogen invasion, this study uses an in vitro approach to isolate the key players and examine the early response of intestinal epithelial cells during infection by T. gondii. We show that human intestinal epithelial cells infected with T. gondii elicit rapid MAPK phosphorylation, NF-κB nuclear translocation, and secretion of interleukin (IL)-8. Both ERK1/2 activation and IL-8 secretion responses were shown to be MyD88 dependent and TLR2 was identified to be involved in the recognition of the parasite regardless of the parasite genotype. Furthermore, we were able to identify additional T. gondii-regulated genes in the infected cells using a pathway-focused array. Together, our findings suggest that intestinal epithelial cells were able to recognize T. gondii during infection, and the outcome is important for modulating intestinal immune responses.
2009-09-17 | GSE18085 | GEO
Project description:The spleen is a site of acute infection following challenge with the parasite Toxoplasma gondii. We utilized scRNA sequencing to analyze the immune response to this infection.
2022-07-01 | GSE207173 | GEO
Project description:Toxoplasma gondii (T. gondii) is an opportunistic parasite. After infection, macrophages finely regulate the immune response to restrict parasite proliferation. It is well-known that N6-methyladenosine (m6A) plays a critical role in fine-tuning gene expression. To investigate whether m6A modification is involved in regulating the anti-infection immune response in macrophages against T. gondii, this study utilized T. gondii tachyzoites from the RH strain to infect human THP-1 macrophages. qPCR and ELISA results showed that T. gondii infection mounted the expression of TNF-α. RNA-seq profiling showed that T. gondii infection was associated with difference in genes from pathway associated with TNF signaling. Expression of m6A regulators were evaluated using qPCR and Western blotting. T. gondii infection increased the abundance of m6A methyltransferase WTAP and demethylase FTO. Joint analysis of RNA-seq and m6A-seq data was utilized for enriching differentially expressed genes with significantly altered m6A modifications. After T. gondii infection, the m6A levels of genes associated with TNF signaling were significantly altered. In this study, we found that m6A methylation involved in T. gondii infection induced TNF-α expression.
2025-07-03 | GSE288205 | GEO
Project description:The apicomplexan parasite Toxoplasma gondii infects a broad range of different cell types in avian and mammalian hosts including humans. Infection of immunocompetent hosts is mostly asymptomatic or benign, but leads to development of largely dormant bradyzoites that persist for the hosts life predominantly within neurons and muscle cells. Here we have analyzed the impact of the host cell type on the co-transcriptomes of host and parasite using high-throughput RNA sequencing. Murine cortical neurons and astrocytes, skeletal muscle cells (SkMCs) and fibroblasts differed by more than 16,200 differentially expressed genes (DEGs) before and at 24 hours after infection with T. gondii. However, only 157 to 492 of these DEGs were regulated within the different cell types by infection. Intriguingly, largely diverse sets of genes were regulated in neurons, SkMCs, astrocytes and fibroblasts following infection indicating host cell type-specific transcriptional responses. Only a few genes were identified that were commonly regulated in two or three host cell types after infection. The heterogeneous transcriptomes of the host cells before and during infection coincided with the differential expression of ~5,400 genes in T. gondii residing in the different host cells. Expression of these DEGs mostly differed quantitatively but within neurons, T. gondii also expressed 121 genes in a strictly host cell-type specific manner. Interestingly, we identified gene clusters in both T. gondii and its host, which correlated with the predominant parasite persistence in neurons or SkMCs as compared to astrocytes or fibroblasts. Thus, heterogeneous expression profiles of different host cell types and the parasites’ ability to adapt to them may govern the parasite-host cell interaction during toxoplasmosis.
2017-08-07 | GSE94595 | GEO
Project description:Toxoplasma gondii is an obligate intracellular parasite which can cause toxoplasmosis. Surface and secreted proteins of T. gondii play important roles in infection and immunity, and also are antigen targets in immunological diagnosis and vaccine development. However, it is difficult to investigate identities and antigenicities of surface and secreted proteins due to limitation of surface protein extraction methods. In this study, a total of 785 potential surface and secreted proteins of T. gondii RH tachyzoites were identified using a method combination of biotin labeling, avidin chromatography isolation, and high flux proteomics (LC-MS/MS). Among the highly-expressed 65 proteins, 43 proteins (66%) were originally annotated as surface or secreted proteins in the released T. gondii genomes, which proved the method combination to be a credible strategy. Furthermore, the transcriptomic responses and cytokine secretions induced by the isolated proteins, the live T. gondii RH tachyzoites infection, and the live pathogenic E. coli infection, in the human peripheral blood monocyte THP-1 cell lines, were comparatively analyzed to reveal antigenicities and immunobiological properties of T. gondii surface and secreted proteins. The transciptomic profiles induced by the isolated proteins were similar to those induced by the live bacterium infection, but were different from those induced by the live parasite infection. Contrary to the low cytokine secretion induced by the live parasite infection, the isolated proteins induced significant cytokine and chemokines secretion. Especially, the secretions of several chemokines induced by the isolated proteins were even higher than those induced by the live bacterium infection. These data suggested that T. gondii surface and secreted proteins were effective antigens, while the live parasite could evade the host innate immunity. This study comprehensively revealed the identities and antigenicities of T. gondii surface and secreted proteins, which laid foundation for further screening new T. gondii antigens, developing immunological diagnosis methods, and studying host immune response to T. gondii infection.
2017-09-20 | GSE103985 | GEO
Project description:Toxoplasma gondii is a globally distributed parasite pathogen that infects virtually all warm-blooded animals. A hallmark of immunity to acute infection is the production of IFN-γ and IL-12, followed by a protective T cell response that is critical for parasite control. Naïve T cell activation requires both TCR stimulation and the engagement of costimulatory receptors. Because of their important function in activating T cells, the expression of co-stimulatory ligands is believed to be under tight control. The molecular mechanisms governing their induction during microbial stimulation, however, are not well understood. We found that all three strains of T. gondii (Types I, II, and III) up-regulated the expression of B7-2, but not B7-1, on the surface of mouse bone marrow-derived macrophages. This induction occurred at the transcriptional level, required active parasite invasion, and was not dependent on MyD88 or TRIF. Genome-wide transcriptional analysis comparing infected and uninfected macrophages revealed the activation of MAPK signaling in infected cells. Using specific inhibitors against MAPKs, we determined that parasite-induced B7-2 is dependent on JNK, but not ERK or p38 signaling. We also observed that T. gondii-induced B7-2 expression on human peripheral blood monocytes is dependent on JNK signaling, indicating that a common mechanism of B7-2 regulation by T. gondii may exist in both humans and mice. We used microarrays to examine genome-wide changes in host cell gene expression during T. gondii infection at an early time point (6 hpi). BMdM were mock-treated or infected with T. gondii (Type I, RH strain) at an MOI of 2 and cultured for 6 hours. Biological triplicates were performed. Total RNA was harvested and used for cDNA synthesis, labeling, and hybridization to Affymetrix mouse 430 2.0 expression arrays.
2011-12-31 | E-GEOD-27972 | biostudies-arrayexpress
Project description:This study utilizes global microarray analysis to identify how T. gondii alters its transcriptome in response to the in vivo microenvironment during the innate immune response (four days post-infection) relative to growth in fibroblast cells in vitro. To distinguish changes in the parasite transcriptome dependent or independent of the host immune response the parasite transcriptome was examined in IFN-gamma gene deleted mice in addition to wild type mice.
2012-07-01 | E-MEXP-3579 | biostudies-arrayexpress