Single cell sequencing of splenocytes following T. gondii infection
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ABSTRACT:
PROVIDER: PRJNA854055 | ENA |
REPOSITORIES: ENA
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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:RNA-seq of mouse splenocytes following infection with Listeria monocytogenes
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Project description:This experiment contains two mice genotypes – WT and Bcl3 flx/flx Zbtb46 cre knockouts (both C57BL/6 background). These mice were either infected with 15 cysts of Toxoplasma gondii (ME49 strain) or kept uninfected. Spleens were harvested from mice 7 days post infection and splenocytes were isolated. With four experimental groups (KO/WT and infected/uninfected) and two biological replicate mice per group, we have a total of 8 biological samples comprising of single cell suspensions of splenocytes enriched for CD11c. Single cell RNA-seq libraries were prepared from CD11c-enriched single cells using the Chromium Single Cell 3’ Reagent Kits v3 (10X Genomics; Pleasanton, CA, USA). Eight sample libraries were multiplexed and sequenced 100bp paired end in four different runs of Illumina NextSeq2000, followed by demultiplexing that resulted in multiple raw FASTQ files corresponding to paired reads (R1 and R2), index barcodes (I1) and four sequencing runs (Seq1 - Seq4). The main goal of this project was to define Bcl3-associated transcriptional responses in dendritic cells during T. gondii infection.
2022-08-08 | GSE193532 | GEO
Project description:Toxoplasma gondii is a protozoan parasite with a remarkable neuro-tropismneurotropic affinity. We recently showed that T. gondii infection can alter the global metabolism of the cerebral cortex of the mice. However, the impact of this infection on the metabolism of the hippocampus remains unclear. In this study, we compared the metabolomic profiles of mouse hippocampus following acute and chronic infection with T. gondii. Our data provide new insight into the neuropathogenesis of T. gondii infection and reveal new pathways and metabolites that mediate the interplay between T. gondii infection and the mouse hippocampus
2021-01-27 | MTBLS1890 | MetaboLights
Project description:Toxoplasma gondii (T. gondii) is an obligate intracellular parasite that can lead to adverse pregnancy outcomes, particularly in early pregnancy. Previous studies have illustrated the landscape of decidual immune cells. However, the landscape of decidual immune cells in the maternal–fetal microenvironment during T. gondii infection remains unknown. In this study, we employed single-cell RNA sequencing to analyze the changes in human decidual immune cells following T. gondii infection. Our results showed that the proportion of 17 decidual immune cell clusters and the expression levels of 21 genes were changed after T. gondii infection. Differential gene analysis demonstrated that T. gondii infection induced the differential expression of 279, 312, and 380 genes in decidual NK, dMφ, and dT cells, respectively. Our findings first revealed that several previously unknown molecules in decidual immune cells changed following T. gondii infection. This result revealed that the function of maternal–fetal immune tolerance declined, whereas the killing ability of decidual immune cells enhanced, eventually contributing to the occurrence of adverse pregnancy outcomes. The results of this study provide a valuable resource for uncovering several novel molecules that play an important role in the occurrence of abnormal pregnancy outcomes induced by T. gondii infection.
2024-05-17 | GSE254302 | 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.
2009-09-17 | GSE18085 | 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:Toxoplasma gondii threats to the health of one-third of the world's population. Cat is the natural definite host of T. gondii. However, the biological changes of feline small intestine following T. gondii infection remains mysterious event. Protein acetylation modification which is a dynamic and reversible post-translational modification (PTM) plays important roles in regulating various physiological functions. In this study, we used affinity enrichment and high resolution LC-MS/MS to analyze the alteration of acetylation event in feline small intestine infected by Prugniuad (Pru) strain of Toxoplasma gondii.
2020-07-09 | PXD018799 | iProX
Project description:Splenocytes comprised a wide-range of immune cells responsible for the protection against infectious diseases. We exposed splenocytes to GFP+ Borrelia, sorted GFP+ and GFP- splenocytes and performed single-cell RNA seq to analyze the DEGs between infected and bystander population in different immune cell populations
2023-11-17 | GSE243126 | GEO
Project description:Retention of lymphocytes in the intestinal mucosa requires specialized chemokine receptors and adhesion molecules. Here we find that both CD4+CD8+ and CD4+T cells in the intestinal epithelium, as well as CD8+T cells in the intestinal mucosa and mesenteric lymph nodes, express the cell adhesion molecule Crtam upon activation, whereas the ligand of Crtam, Cadm1, is expressed on gut CD103+DCs. Lack of Crtam-Cadm1 interactions in Crtam-/- and Cadm1-/- mice results in loss of CD4+CD8+T cells, which arise from mucosal CD4+T cells that acquire a CD8 lineage expression profile. Following acute oral infection with T. gondii, both WT and Crtam-/- mice mounted a robust TH1 response, but markedly fewer TH17 cells were present in the intestinal mucosa of Crtam-/- mice. The almost exclusive TH1 response in Crtam-/- mice resulted in more efficient control of intestinal T. gondii infection. CD4+ T cells were cell sorted to analyze the differences resulting from the lack of Crtam expression during T. gondii infection.
2014-02-15 | E-GEOD-55067 | biostudies-arrayexpress