Homo sapiens
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PROVIDER: PRJNA141925 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of the human endothelial cell response to Borrelia burgdorferi wild-type and deleted in the gene encoding the integrin ligand P66 [experiment A]
| PRJNA141825 | ENA
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.
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: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 etiological agent of Lyme disease, persists in nature through an enzootic cycle consisting of a vertebrate host and an Ixodes tick vector. The sequence motifs modified by two well-characterized restriction/modification loci of B. burgdorferi type strain B31 were recently described, but the methylation profiles of other Lyme disease Borrelia have not been characterized. Herein, the methylomes of B. burgdorferi type strain B31 and 7 clonal derivatives, along with B. burgdorferi N40, B. burgdorferi 297, B. burgdorferi CA-11, B. afzelii PKo, B. afzelii BO23, and B. garinii PBr, were defined through PacBio SMRT sequencing. This analysis revealed 9 novel sequence motifs methylated by the plasmid-encoded restriction/modification enzymes of these Borrelia strains. Furthermore, while a previous analysis of B. burgdorferi B31 revealed an epigenetic impact of methylation on the global transcriptome, the current data contradict those findings; our analyses of wild-type B. burgdorferi B31 revealed no consistent differences in gene expression among isogenic derivatives lacking one or more restriction/modification enzyme(s).
2021-03-24 | GSE169460 | GEO
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:The pathogenic spirochete Borrelia burgdorferi senses and responds to diverse environmental challenges, including changes in nutrient availability, throughout its natural infectious cycle in Ixodes spp. ticks and mammalian hosts. This study examined the role of the putative DnaK suppressor protein (DksA) in the transcriptional response of B. burgdorferi to starvation. Wild-type and dksA-deficient B. burgdorferi strains were subjected to starvation by shifting mid-logarithmic cultures grown in BSK-II medium to serum-free RPMI medium for six hours under microaerobic conditions (5% CO2, 3% O2). Microarray analyses of wild-type B. burgdorferi revealed that genes encoding flagellar components, ribosomal proteins, and DNA replication machinery were downregulated in response to starvation. DksA mediated transcriptomic responses to starvation in B. burgdorferi as the dksA-deficient B. burgdorferi strain differentially expressed only 47 genes in response to starvation compared to the 500 genes differentially expressed by wild-type strains. Consistent with a role for DksA in the starvation response of B. burgdorferi, fewer CFUs were observed for dksA-deficient spirochetes after prolonged starvation in RPMI medium compared to wild-type B. burgdorferi. Transcriptomic analyses revealed a partial overlap between the DksA regulon and the regulon of the guanosine tetraphosphate and guanosine pentaphosphate [(p)ppGpp] synthase RelBbu, while the DksA regulon also included many plasmid-borne genes. Corresponding to a DksA-(p)ppGpp regulatory relationship, (p)ppGpp levels were constitutively elevated in the dksA-deficient strain compared to the wild-type strain. Together, these data indicate that DksA directs the stringent response with a regulatory interplay with (p)ppGpp that is fundamental to B. burgdorferi responses to the environment.
2018-12-18 | GSE119023 | 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