Transcriptome analysis of human brain microvascular endothelial cells response to Borrelia burgdorferi and its antigen Erp23 using RNA-seq
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PROVIDER: PRJEB33005 | ENA |
REPOSITORIES: ENA
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Project description:Using RNA sequencing to map differentially expressed genes in human brain microvascular endothelial cells challenged with Borrelia burgdorferi or its ligand Erp23.
2019-06-21 | E-MTAB-8053 | biostudies-arrayexpress
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:Borrelia burgdorferi, the agent of Lyme disease, promotes pro-inflammatory changes in endothelium that lead to the recruitment of leukocytes. The host immune response to infection results in increased levels of IFN-gamma in the serum and lesions of Lyme disease patients that correlate with greater severity of disease. Therefore, the effect of IFN-gamma on the gene expression profile of primary human endothelial cells exposed to B. burgdorferi was determined. B. burgdorferi and IFN-gamma synergistically augmented the expression of 34 genes, seven of which encode chemokines. Six of these (CCL7, CCL8, CX3CL1, CXCL9, CXCL10, and CXCL11) attract T lymphocytes, and one (CXCL2) is specific for neutrophils. Synergistic production of the attractants for T cells was confirmed at the protein level. IL-1beta, TNF-alpha, and LPS also cooperated with IFN-gamma to induce synergistic production of CXCL10 by endothelium, indicating that IFN-gamma potentiates inflammation in concert with a variety of mediators. An in vitro model of the blood vessel wall revealed that an increased number of human T lymphocytes traversed endothelium exposed to B. burgdorferi and IFN-gamma, as compared to unstimulated endothelial monolayers. In contrast, addition of IFN-gamma diminished the migration of neutrophils across B. burgdorferi-activated endothelium. IFN-gamma thus alters gene expression by endothelium exposed to B. burgdorferi in a manner that promotes recruitment of T cells and suppresses that of neutrophils. This modulation may facilitate the development of chronic inflammatory lesions in Lyme disease. Experiment Overall Design: Human umbilical vein endothelial cells (HUVEC) were stimulated with Interferon-gamma (IFN-g), Borrelia burgdorferi or both IFN-g and Borrelia or were left unstimulated. Affymetrix HGU133 plus 2.0 slides were used in duplicate for each condition.
2008-06-14 | E-GEOD-6092 | biostudies-arrayexpress
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:RNA was isolated from late-log pahse wild-type Borrelia burgdorferi B31 and the bb0647 mutant grown in BSKH media at 37 degree, 5% CO2. cDNA was synthesized, labeled and hybridized to the 70mer oligonucleotide B. burgdorferi array. Slides were scanned using axon scanner and image were analyzed using GenePix 6.0. Dta were further analysed using the professional software Acuity 4.o, based on a ratio-based normalization. Samples were labeled by either Cy3 or Cy5. 5 hybs were performed, including dye-swaps.
2010-05-15 | E-GEOD-17422 | biostudies-arrayexpress
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:RNA was isolated from late-log pahse wild-type Borrelia burgdorferi B31 and the bb0647 mutant grown in BSKH media at 37 degree, 5% CO2. cDNA was synthesized, labeled and hybridized to the 70mer oligonucleotide B. burgdorferi array. Slides were scanned using axon scanner and image were analyzed using GenePix 6.0. Dta were further analysed using the professional software Acuity 4.o, based on a ratio-based normalization.
2010-01-20 | GSE17422 | GEO
Project description:Differential gene expression analysis was performed to assess the affects of the deletion of sRNA SR0726 on the in vitro transcriptome of Borrelia burgdorferi in order to investigate a potential regulatory role for the sRNA
2022-02-27 | GSE197340 | GEO
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: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