RNA-seq reveals changes in the astrocyte transcriptome following Borrelia burgdorferi infection
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE85143 | GEO | 2017/02/01
SECONDARY ACCESSION(S): PRJNA336335
REPOSITORIES: GEO
Similar Datasets
Project description:miRNA profiles of astrocytes infected with Borrelia burgdorferi for 24 hours, 48 hours, and 24 hour uninfected controls were generated by deep sequencing, in duplicate, using Illumina MiSeq.
2017-02-01 | GSE85142 | GEO
Project description:The overall goal of these experiments was to determine how human cells respond to ontegrin binding by Borrelia burgdorferi. Lyme disease is the most common vector-borne infection in the Northern hemisphere, yet little is understood about the pathogenic mechanisms of the causative agent, Borrelia burgdorferi. Cells in culture were infected with the bacteria that do and do not express the beta3 integrin ligand P66, which are otherwise isogenic. As additional controls, uninfected cells were also included in the analyses. The cell line used for primary data analyses provided here was Ea.hy926, a macrovascular line (Edgell, C. J.,et al. 1990. Endothelium specific Weibel-Palade bodies in a continuous human cell line, EA.hy926. In vitro Cell. & Dev. Biol. 26:1167-1172, and Edgell, C. J., et al. 1983. Permanent cell line expressing human factor VIII-related antigen established by hybridization. Proc. Natl. Acad. Sci. 80:3734-3737). In addition, the human microvascular endothelial cell line HMEC (Ades et al, 1992. HMEC-1: establishment of an immortalized human microvascular endothelial cell line. J Invest Dermatol. 99:683-690) was used. Epithelial cells HEK-293 (which does not express b3 integrins) and HEK-293 transfected to express integrin ?v?3 were also analyzed. Infection times were 1 hour or 3 hours for cells lifted with EDTA and washed prior to bacterial infection, or 3, 6, and 24 hours for samples in which the bacteria were added to adherent cells. RNA was harvested and reverse transcribed. Labeled cDNAs were used to probe 2 color arrays. In each of at least three biological replicate experiments, for each time point, the following comparisons were made. First, cells infected with B. burgdorferi with a marker inserted adjacent to the p66 gene (p66+) were compared to uninfected cells. Second, cells infected with the p66 gene interrupted by the marker (Coburn, J. and Cugini, C. (2003) Targeted mutation of P66 of Borrelia burgdorferi disrupts attachment to integrin ?v?3. Proc. Natl. Acad. Sci. 100:7301-7306) the mutant-infected cells were compared to the uninfected cells. In some experiments, cells infected with p66+ were compared to cells infected with the p66- mutant. Arrays used were HEEBO arrays purchased from Microarrays Inc. (Nashville, TN). Ea.hy926 or HMEC endothelial cell lines, or HEK-293 epithelial cells, or transfected HEK-293 derivative expressing integrin avb3
2011-03-18 | E-GEOD-27252 | biostudies-arrayexpress
Project description:Lyme disease (LD) is one of the most important human vector-borne diseases in North America. Since transmission of Borrelia burgdorferi (Bb), the causative agent of LD, is influenced by yet unknown tick saliva proteins (TSP), the discovery and characterization of such TSPs are highly sought after for their potential as tick-antigen based vaccine targets. We validated a novel non-invasive approach of collecting sufficient amounts of saliva from unfed, partially fed (12, 24, 36, 48, 60, and 72h), and replete fed Ixodes scapularis nymphs for identification of tick saliva proteins using the LC-MS/MS approach. Our data has described TSPs that might be injected into the host within few hours of the tick starting to feed and are likely associated with manipulating host immunity to facilitate transmitted Bb to colonize the host. Thus, these data will serve as a source for Bb-infection associated TSPs that might be targeted in tick-antigen based vaccines to prevent LD. Equally important, the non-invasive method to collect nymph tick saliva is likely to provide transformative impact on research to understand transmission of other TBD agents.
2021-09-10 | PXD023940 | Pride
Project description:The overall goal of these experiments was to determine how human cells respond to ontegrin binding by Borrelia burgdorferi. Lyme disease is the most common vector-borne infection in the Northern hemisphere, yet little is understood about the pathogenic mechanisms of the causative agent, Borrelia burgdorferi. Cells in culture were infected with the bacteria that do and do not express the beta3 integrin ligand P66, which are otherwise isogenic. As additional controls, uninfected cells were also included in the analyses.
2011-03-18 | GSE27995 | GEO
Project description:The overall goal of these experiments was to determine how human cells respond to ontegrin binding by Borrelia burgdorferi. Lyme disease is the most common vector-borne infection in the Northern hemisphere, yet little is understood about the pathogenic mechanisms of the causative agent, Borrelia burgdorferi. Cells in culture were infected with the bacteria that do and do not express the beta3 integrin ligand P66, which are otherwise isogenic. As additional controls, uninfected cells were also included in the analyses.
2011-03-18 | GSE27252 | GEO
Project description:Lyme disease is a result from an infection by the spirochete Borrelia burgdorferi, and is the leading vector-borne disease in North America. Due to the genomic and proteomic variability of different B. burgdorferi isolates, the study and further comparison of their proteome is key to understand the biology and infectivity of these spirochetes. Mass spectrometry-based proteomics was used to assemble peptide datasets of laboratory isolates B31, MM1, B31-ML23, and the infective isolates B31-5A4, B31-A3, and 297, as well as other public datasets, and is publicly available as the Borrelia PeptideAtlas (http://www.peptideatlas.org/builds/borrelia/). These datasets include information on total proteome, secretome, and membrane proteome of the B. burgdorferi.
2024-09-03 | PXD046281 | Pride
Project description:Purpose: When we infect human dermal microvascular endothelial cells (HMEC-1) infected or not with Borrelia burgdorferi (MOI= 200 bacteria/cell) and examine the host cell kinematics and dynamics over the course of 3 days post-infection we observe a change in those at early times post-infection, but at late times (> 20 h post-infection) cells from infected or not wells behave similarly. To get a sense of the biochemical signals that might be driving the changes in host cell mechanics, we performed RNA-Sequencing and gene expression profiling for uninfected HMEC-1 cells or cells infected for 4, 24 or 48 h with Borrelia burgdorferi at an MOI of 200 bacteria/cell. Methods and Results: By analyzing the differentially expressed genes between all conditions we find a significant number of up- or down-regulated genes infected and uninfected cells just at 4 h post-infection. Through pathway enrichemnet analysis we find that compared to cells not exposed to infection infected cells showed significant upregulation to genes related IL-17 and NF-kB and TNF related signaling pathways. Interestingly these changes are not present at 24 or 48 h post-infection where cells from infected wells are more similar gene expression-wise to uninfected cells. Conclusions: The changes in kinematics and dynamics of HMEC-1 cells exposed to Borrelia burgdorferi (MOI= 200 bacteria/cell) at early times post-infection are associated with changes in innate immune signaing of the host cells. At later times post-infection were these changes in gene expression are not present anymore, host cell kinematics and dynamics are identical between infected and uninfected cells. Thus it is possible that innate immune singaling might be underlying the changes that host cells undergo in their motion and traction forces at early infection.
2021-05-18 | GSE174545 | GEO
Project description:The aim of the study was to compare the global transcriptional responses elicited in NHDF cells by three different strains of Borrelia burgdorferi ss (the agent of Lyme borreliosis), representative of different stages in the life cycle of Borrelia: one reference strain isolated from a tick (strain N40), and two invasive strains isolated from skin biopsy of erythema migrans (strain Pbre c4) and acrodermatitis chronica atrophians skin lesions (strain 1408 c1). Three different experimental conditions have been tested: (1) unstimulated NHDF vs NHDF stimulated by Borrelia strain N40 / (2) unstimulated NHDF vs NHDF stimulated by Borrelia strain Pbre c4 / (3)M-BM- unstimulated NHDF vs NHDF stimulated by Borrelia strain 1408 c1. There is 2 biological replicates for each condition. All NHDF stimulation have been performed in independent experiments.
2012-08-01 | E-GEOD-31740 | biostudies-arrayexpress
Project description:Background: Lyme borrelia genotypes differ in their capacity to cause disseminated disease. Gene array analysis was employed to profile the host transcriptome induced by Borrelia burgdorferi strains with different capacities for causing disseminated disease in the blood of C3H/HeJ mice during early infection. Results: Borrelia burgdorferi B515, a clinical isolate that causes disseminated infection in mice, differentially regulated 236 transcripts (P<0.05 by ANOVA, with fold change of at least 2). The 216 significantly induced transcripts included IFN-responsive genes and genes involved in immunity and inflammation. In contrast, B. burgdorferi B331, a clinical isolate that causes transient skin infection but does not disseminate in C3H/HeJ mice, stimulated changes in only a few genes (1 induced, 4 repressed). Transcriptional regulation of type I IFN and IFN-related genes was measured by quantitative RT-PCR in mouse skin biopsies collected from the site of infection 24 hours after inoculation with B. burgdorferi. The mean values for transcript of Ifnb, Cxcl10, Gbp1, Ifit1, Ifit3, Irf7, Mx1, and Stat2, were found to be significantly increased in B. burgdorferi strain B515-infected mice relative to the control group. In contrast, transcription of these genes was not significantly changed in response to B. burgdorferi strain B331 or B31-4, a mutant that is unable to disseminate. Conclusions: These results establish a positive association between the disseminating capacity of B. burgdorferi and early type I IFN induction in a murine model of Lyme disease.
2016-03-25 | E-MTAB-3325 | biostudies-arrayexpress
Project description:Borrelia burgdorferi species complex population genomics study with the focus on Borrelia garinii.
| PRJNA662729 | ENA