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Global transcriptome analysis of B. burgdorferi during adherence and invasion of human neuroglial cells

ABSTRACT: As adherence and entry of a pathogen into a host cell are two key components to an infection, identifying the molecular mechanisms responsible for cellular association will provide a better understanding of a microbe’s ability for pathogenesis. We previously established an in vitro model for B. burgdorferi invasion of human neuroglial cells. To expand on our earlier study, we performed B. burgdorferi whole-genome expression analysis following a 20-hour infection of human neuroglial cells to identify borrelial genes that were differentially regulated during cellular attachment and invasion as compared with cultured Borrelia in cell-free medium. This study identifies several regulated genes, the products of which may be important mediators for cellular pathogenesis. Keywords: in-vitro H4 neuroglial cells infected with B. burgdorferi

ORGANISM(S): Coxiella burnetii Chlamydia trachomatis Yersinia pestis Streptococcus pyogenes Staphylococcus aureus Homo sapiens Borreliella burgdorferi

PROVIDER: GSE8219 | GEO | 2008/06/20

SECONDARY ACCESSION(S): PRJNA101141

REPOSITORIES: GEO

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Global transcriptome analysis of B. burgdorferi during adherence and invasion of human neuroglial cells

Project description:As adherence and entry of a pathogen into a host cell are two key components to an infection, identifying the molecular mechanisms responsible for cellular association will provide a better understanding of a microbeâs ability for pathogenesis. We previously established an in vitro model for B. burgdorferi invasion of human neuroglial cells. To expand on our earlier study, we performed B. burgdorferi whole-genome expression analysis following a 20-hour infection of human neuroglial cells to identify borrelial genes that were differentially regulated during cellular attachment and invasion as compared with cultured Borrelia in cell-free medium. This study identifies several regulated genes, the products of which may be important mediators for cellular pathogenesis. Keywords: in-vitro H4 neuroglial cells infected with B. burgdorferi A 20-hour incubation was performed, and this time point included B. burgdorferi that were both intra- and extra-cellularly localized to the H4 cells (Livengood and Gilmore, 2006). After B. burgdorferi infection of these cells, the total cellular RNA preparation (including H4 RNA, and Borrelia RNA) was enriched for prokaryotic RNA, which concentrated the bacterial message, but did not completely eliminate the eukaryotic RNA (data not shown). Therefore, as a control in our arrays, eukaryotic RNA from the human H4 cells was also purified and hybridized to the array. To control for Borrelia cell-free gene expression, the data from the experimental conditions (B. burgdorferi infected human cells) was normalized to borrelial expression following growth in BSK and a 20 hour incubation in DMEM tissue culture media. As with the experimental samples, both controls were assayed in triplicate.

2010-05-26 | E-GEOD-8219 | biostudies-arrayexpress

Identification of the differences between gene expression in normal human dermal fibroblasts (NHDF cell line) infected with Borrelia burgdorferi sensu lato spirochetes

Project description:The similarity of Lyme borreliosis to other diseases and the complex pathogenesis cause diagnostic and therapeutic difficulties. Changes at the cellular and molecular level after Borrelia sp. infection remain still poorly understood. Therefore, the present study focused on the gene expression in human dermal fibroblasts in differentiation of infection with Borrelia garinii, Borrelia afzelii and Borrelia burgdorferi sensu stricto spirochetes. For microarray analysis 10 samples were used: 3 control samples - K, 2 samples of NHDF cells infected with Borrelia garinii - G, 2 samples of NHDF cells infected with Borrelia afzelii - A and 3 samples of NHDF cells infected with Borrelia burgdorferi sensu stricto - SS.

2015-05-12 | E-GEOD-68741 | biostudies-arrayexpress

Global transcriptome analysis of B. burgdorferi during adherence and invasion of human neuroglial cells

Project description:Global transcriptome analysis of B. burgdorferi during adherence and invasion of human neuroglial cells

| PRJNA101141 | ENA

Identification of the differences between gene expression in normal human dermal fibroblasts (NHDF cell line) infected with Borrelia burgdorferi sensu lato spirochetes

2015-05-12 | GSE68741 | GEO

Single-cell transcriptome analysis of the early immune response in the lymph nodes of Borrelia burgdorferi-infected mice

Project description:Lyme borreliosis is a disease caused by Borrelia burgdorferi sensu lato bacteria. Borrelia burgdorferi is known to induce prolonged extrafollicular immune responses and abnormal germinal center formation. However, the mechanism behind this is poorly understood. The extrafollicular response is characterized by strong plasmablast induction and by an IgM, IgG3, and IgG2b dominant antibody production. These antibodies do not generate a neutralizing type of immunity, and the bacteria eventually establish a persistent infection. Here, we performed single-cell RNA sequencing to characterize the immune landscape of lymph node lymphocytes in the early Borrelia burgdorferi infection in a murine model.

2024-09-19 | GSE248267 | GEO

Borrelia burgdorferi induces a type I interferon response during early stages of disseminated infection in mice

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

Borrelia PeptideAtlas: A proteome resource of common Borrelia burgdorferi isolates for Lyme community

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

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Project description:Borrelia burgdorferi Genome sequencing

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The Lyme disease bacterium, Borrelia burgdorferi, stimulates an inflammatory response in human choroid plexus epithelial cells

Project description:We report the results of gene expression profiling via RNA-sequencing of primary human choroid plexus epithelial cells in vitro that were infected with Borrelia burgdorferi, the causative agent of Lyme disease. Epithelial cells were cultured with B. burgdorferi for 48 hours prior to RNA isolation. Following high-throughput sequencing via Illumina HiSeq 4000, a total of 258 differentially expressed genes were identified. Subsequent data analysis indicates an inflammatory and immune response generated by the epithelial cells following infection, marked by chemotactic cytokines and interferon stimulated genes. Several genes associated with tight and adherens junctions were found to be downregulated. These data represent the first study to investigate the impact of B. burgdorferi on choroid plexus epithelial cells, implicating the choroid plexus in the pathogenesis of neurological manifestations of Lyme disease.

2020-07-10 | GSE153261 | GEO

Analysis of the human endothelial cell response to Borrelia burgdorferi wild-type and deleted in the gene encoding the integrin ligand P66 [experiment A]

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

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