Scavenger receptors on the cell surface of macrophages play an important role in host defence through their ability to bind microbial ligands and induce phagocytosis. Concurrently, signal transduction pathways are initiated that aid in defence mechanisms against the invading microbe. Here we report on the function of scavenger receptor Marco (macrophage receptor with collagenous structure) during infection of zebrafish embryos with Mycobacterium marinum, a close relative of Mycobacterium tuberculosis. Morpholino knockdown demonstrates that Marco is required for the rapid phagocytosis of M. marinum following intravenous infection. Furthermore, gene expression analysis shows that Marco controls the initial transient pro-inflammatory response to M. marinum and remains a determining factor for the immune response signature at later stages of infection. Increased bacterial burden following marco knockdown indicates that this scavenger receptor is important for control of M. marinum growth, likely due to delayed phagocytosis and reduced pro-inflammatory signalling observed under conditions of Marco deficiency Overall design: Embryos were injected at the one cell stage with a morpholino targeting marco, or with the standard control morpholino from GeneTools for comparison. Subsequently, at 24 hours post fertilization (hpf) the morphants and their controls were manually dechorionated at 24 hpf and at 28 hpf they were infected by injecting 200 colony forming units of M. marinum Mma20 into the caudal vein, or mock-injected with PBS/2%PVP. After injections embryos were transferred into fresh egg water containing 0.003% 1-phenyl-2-thiourea (Sigma-Aldrich) to prevent melanization and incubated for 4 days at 28°C. After the incubation period, infected and uninfected morphants, mutants and their controls were imaged and groups of 30 embryos were snap-frozen in liquid nitrogen and RNA was isolated for Illumina RNAseq analysis.
Phagocytosis of mycobacteria by zebrafish macrophages is dependent on the scavenger receptor Marco, a key control factor of pro-inflammatory signalling.
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View SamplesComparison of gene expression profile of E. coli 83972 grown in minimal lab media, in urine and in 3 individual patients.
Global gene expression profiling of the asymptomatic bacteriuria Escherichia coli strain 83972 in the human urinary tract.
No sample metadata fields
View SamplesIdentification of genes differentially expressed in roots of Arabidopsis Col-0 and ndr1-1 mutants 48 h post inoculation with the fungal pathogen Verticillium longisporum.
Susceptibility to Verticillium longisporum is linked to monoterpene production by TPS23/27 in Arabidopsis.
Age, Specimen part, Time
View SamplesDetection of single feature polymorphisms comparing five barley genotypes. Gene expression under unstressed and drought stressed conditions.
Detecting single-feature polymorphisms using oligonucleotide arrays and robustified projection pursuit.
No sample metadata fields
View SamplesThe in vitro effect of infection with different strains of Toxoplasma gondii was tested 24 hours after infection of Human Foreskin Fibroblasts (HFF)
Integrative genomic approaches highlight a family of parasite-specific kinases that regulate host responses.
No sample metadata fields
View SamplesWe used microarray to compare global gene expression profiles between 5 GNAQ/11 mutant uveal melanoma cell lines (GNAQ mutant: 92-1, omm1.3, mel270; GNA11 mutant: omm-gn11 and upmd-1) and 5 GNAQ/11 wild type melanoma cell lines(sk-mel-2, mm415, mm485, sk-mel-5 and mum2c). Uveal melanoma is the most common intraocular tumor that mainly metastasizes to the liver in about 50% patients. Over 80% of UMs harbor GNAQ or GNA11 activating mutation. Currently there is no effective treatment available for UM patients. Results provide insights into downstream signaling of oncogenic GNAQ/11 and identification of therapeutic targets in UM.
RasGRP3 Mediates MAPK Pathway Activation in GNAQ Mutant Uveal Melanoma.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Differential induction of TLR3-dependent innate immune signaling by closely related parasite species.
Specimen part, Cell line
View SamplesThe closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II () interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (/) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits TLR3-dependent type I interferon responses when targeted to the host endo-lysosomal system. Although live Toxoplasma fail to induce type I interferon, heat-killed parasites do trigger this response, albeit much weaker than Neospora, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that related parasite species interact with this pathway in distinct ways.
Differential induction of TLR3-dependent innate immune signaling by closely related parasite species.
Specimen part, Cell line
View SamplesThe closely related protozoan parasites Toxoplasma gondii and Neospora caninum display similar life cycles, subcellular ultrastructure, invasion mechanisms, metabolic pathways, and genome organization, but differ in their host range and disease pathogenesis. Type II () interferon has long been known to be the major mediator of innate and adaptive immunity to Toxoplasma infection, but genome-wide expression profiling of infected host cells indicates that Neospora is a potent activator of the type I (/) interferon pathways typically associated with antiviral responses. Infection of macrophages from mice with targeted deletions in various innate sensing genes demonstrates that host responses to Neospora are dependent on the toll-like receptor Tlr3 and the adapter protein Trif. Consistent with this observation, RNA from Neospora elicits TLR3-dependent type I interferon responses when targeted to the host endo-lysosomal system. Although live Toxoplasma fail to induce type I interferon, heat-killed parasites do trigger this response, albeit much weaker than Neospora, and co-infection studies reveal that T. gondii actively suppresses the production of type I interferon. These findings reveal that eukaryotic pathogens can be potent inducers of type I interferon and that related parasite species interact with this pathway in distinct ways.
Differential induction of TLR3-dependent innate immune signaling by closely related parasite species.
Specimen part
View SamplesBackground: The use of electrical pulses to enhance uptake of molecules into living cells have been used for decades. This technique, often referred to as electroporation, has become an increasingly popular method to enhance in vivo DNA delivery for both gene. therapy applications as well as for delivery of vaccines against both infectious diseases and cancer. In vivo electrovaccination is currently being investigated in several clinical trials, including DNA delivery to healthy volunteers. However, the mode of action at molecular level is not yet fully understood.
Skin electroporation: effects on transgene expression, DNA persistence and local tissue environment.
Specimen part
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