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Immunobiology and natural history of human infection with agent of Lyme disease, Borrelia burgdorferi

ABSTRACT: Immunobiology and natural history of human infection with agent of Lyme disease, Borrelia burgdorferi

PROVIDER: PRJNA802947 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR18598928_1.fastq.gz	Fastqsanger.gz
	SRR18598928_2.fastq.gz	Fastqsanger.gz
	SRR18598929_1.fastq.gz	Fastqsanger.gz
	SRR18598929_2.fastq.gz	Fastqsanger.gz

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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

Transcription profiling of human umbilical vein endothelial cells treated with Interferon-gamma (IFN-g), Borrelia burgdorferi or both IFN-g and Borrelia or untreated to investigate immune responses to Lyme disease

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

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

Borrelia burgdorferi, the Lyme disease spirochete, possesses genetically-encoded responses to doxycycline, but not to amoxicillin.

Project description:Purpose: To determine whether Borrelia burgdorferi, the spirochetal agent of Lyme disease, responds to sub-lethal doses of antibiotics. Methods: mRNA profiles of Borrelia burgdorferi were compared after subculturing in 0.2μg/mL amoxicillin, 0.2μg/mL doxycycline, or media control for 3h or 24h (n=3 per group) by paired-end sequencing using the Illumina NextSeq 500. The sequence reads were aligned using Salmon aligner followed by DESeq2 for differential expression analysis. Results: After culturing for 24 h in a sub-lethal concentration of doxycycline, there were significant increases in a substantial number of transcripts for proteins that are involved with translation. Bacteria continued to elongate, but appeared to be defective in septation and formed filaments. In contrast, incubation with sublethal concentration of amoxicillin led to membrane blebbing and swelling, indicative of cell wall disruption, but no significant changes in levels of any bacterial transcript. Conclusion: We conclude that B. burgdorferi has a mechanism(s) that detects translational inhibition by doxycycline, and increases production of translational machinery in compensation. In contrast, The absence of response to the inhibition of cell wall synthesis by amoxicillin implies that B. burgdorferi lacks a mechanism to assess cell wall integrity.

2022-03-08 | GSE197338 | 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

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

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

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2024-09-19 | GSE248267 | GEO

Tick Adiponectin Receptor-Mediated Phospholipid Metabolism Contributes to Borrelia burgdorferi Colonization

Project description:Adiponectin-mediated pathways contribute to mammalian homeostasis; however, little is known about adiponectin and adiponectin receptor signaling in arthropods. In this study, we demonstrate that Ixodes scapularis ticks have an adiponectin receptor-like protein (ISARL) but lack adiponectin, suggesting activation by alternative pathways. ISARL expression is significantly upregulated in the tick gut after Borrelia burgdorferi infection, suggesting that ISARL signaling may be co-opted by the Lyme disease agent. Consistent with this, RNA interference (RNAi)-mediated silencing of ISARL significantly reduced the B. burgdorferi burden in the tick. RNA-seq-based transcriptomics and RNAi assays demonstrate that ISARL-mediated phospholipid metabolism by phosphatidylserine synthase I is associated with B. burgdorferi survival. Furthermore, the tick complement C1q-like protein 3 interacts with ISARL, and B. burgdorferi facilitates this process. This study identifies a new tick metabolic pathway that is connected to the life cycle of the Lyme disease spirochete.

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Transcriptional responses of normal human dermal fibroblasts (NHDF) induced by Borrelia burgdorferi sensu stricto

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).

2012-08-02 | GSE31740 | GEO

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