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Macrophage training to Borrelia burgdorferi governs cardiac inflammation in the mammalian host [RNA-seq]

ABSTRACT: Macrophage training to Borrelia burgdorferi governs cardiac inflammation in the mammalian host [RNA-seq]

PROVIDER: PRJNA516652 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8477840.fastq.gz	Fastqsanger.gz
	SRR8477841.fastq.gz	Fastqsanger.gz
	SRR8477842.fastq.gz	Fastqsanger.gz
	SRR8477843.fastq.gz	Fastqsanger.gz
	SRR8477844.fastq.gz	Fastqsanger.gz

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Macrophage training to Borrelia burgdorferi governs cardiac inflammation in the mammalian host

Project description:Macrophage training to Borrelia burgdorferi governs cardiac inflammation in the mammalian host

| PRJNA516655 | ENA

Macrophage training to Borrelia burgdorferi governs cardiac inflammation in the mammalian host [RNA-seq]

Project description:Macrophage exposure to vaccine or vaccine-like formulations results in disparate secondary responses. We have identified the transcriptomic and metabolic changes associated with the memory response of macrophages to Borrelia burgdorferi, an extracellular pathogen able to establish long-term infections in mammals. Memory macrophages show an enhanced ability to bind and internalize the spirochete with decreased inflammatory responses, in part regulated by Irf4. Experienced macrophages also show an augmented glycolytic output. In vivo, glycolysis inhibition results in decreased cardiac inflammation and reduced expression of Irf4. Our data show that B. burgdorferi induces long-term, memory-like responses that are amenable to be manipulated in vivo.

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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.

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microRNA changes in astrocytes following Borrelia burgdorferi infection

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.

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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

Transcriptional profiling of the Borrelia burgdorferi bb0647 mutant

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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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Project description:Borrelia burgdorferi B31 derivative strain ML23 and SR0736 sRNA mutant grown in vitro in mammalian-like conditions 37C, 5%CO2, pH 6.8

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