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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse joint tissue from C3H and interval specific congenic mouse lines post- B. burgdorferi infection

ABSTRACT: Gene expression profile of joint tissue from C3H and interval specific congenic mouse lines (ISCL) following infection with Borrelia burgdorferi; Congenic lines of mice generated between C3H and C57BL/6 with penetrant arthritis severity phenotype were infected with B. burgdorferi; Joint tissue was collected from uninfected control mice and from mice infected for 1 week, RNA was prepared and gene expressed analyzed by Affymetrix microarray. Experiment Overall Design: Each sample was comprised of pooled RNA from at least 5 female mice of each genotype.

ORGANISM(S): Mus musculus

SUBMITTER: Janis Weis

PROVIDER: E-GEOD-16195 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Interval-specific congenic lines reveal quantitative trait Loci with penetrant lyme arthritis phenotypes on chromosomes 5, 11, and 12.

Ma Ying Y Miller Jennifer C JC Crandall Hillary H Larsen Eric T ET Dunn Diane M DM Weiss Robert B RB Subramanian Meenakumari M Weis John H JH Zachary James F JF Teuscher Cory C Weis Janis J JJ

Infection and immunity 20090601 8

The observation that Borrelia burgdorferi-induced arthritis is severe in C3H mice and milder in C57BL/6 (B6) mice has allowed a forward genetics approach for the identification of genetic elements that regulate the arthritis response. Quantitative trait loci (QTL) on five chromosomes (Chr) were identified previously in segregating crosses between C3H and B6 mice and collectively designated B. burgdorferi arthritis-associated (Bbaa) QTL. Reciprocal interval-specific congenic lines (ISCL) that enc ...[more]

PMID: 19487472

Similar Datasets

Expression profiling of joint tissue from C3H and interval specific congenic mouse lines post- B. burgdorferi infection

Project description:Gene expression profile of joint tissue from C3H and interval specific congenic mouse lines (ISCL) following infection with Borrelia burgdorferi Congenic lines of mice generated between C3H and C57BL/6 with penetrant arthritis severity phenotype were infected with B. burgdorferi Joint tissue was collected from uninfected control mice and from mice infected for 1 week, RNA was prepared and gene expressed analyzed by Affymetrix microarray.

2009-06-22 | GSE16195 | 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

The Cdkn2a gene product ARF is a critical regulator of IFNb mediated Lyme arthritis

Project description:Lyme disease is caused by infection with Borrelia burgdorferi, with a spectrum of clinical disorders. Murine studies with B6 and C3H mice have demonstrated that genetic differences in the host response play an essential role in regulating the severity of Lyme arthritis. C3H mice generate a robust induction of type I IFN response in joint tissue at one week of infection which leads to severe Lyme arthritis at 4 weeks post-infection, while B6 mice develop mild disease without a type I IFN profile. We used a forward genetic approach and identified B. burgdorferi arthritis- associated locus 1 (Bbaa1) on Chr4, which includes type I IFN cluster. B6.C3-Bbaa1 congenic mice display more severe Lyme arthritis than B6 mice. The blocking of type I IFN receptor and the IFNb subtype in Bbaa1 mice suppressed arthritis back to B6 level, so we concluded the Bbaa1 locus intrinsically controls IFNb production, and the differential expression of IFNb controls the severity of Lyme arthritis. However, the IFNb genes of C3H and B6 mice are identical, prompting focus on other genetic factors within the Bbaa1 locus as regulators of IFNb. Reciprocal radiation chimeras between B6.C3-Bbaa1 and B6 mice revealed myeloid cells in the joint tissue as IFNb initiators. Advanced congenic lines were generated to reduce the genetic contribution from C3H Bbaa1 region. RNA-seq of bone marrow-derived macrophages (BMDMs) from B6 and advanced interval specific recombinant congenic lines, ISRCL3 and ISRCL4, revealed novel candidates that may regulate Ifnb. In this study, we identify the Cdkn2a gene encoded ARF as a critical regulator of IFNb mediated Lyme arthritis, and investigate mechanistic interactions that modulate IFNb expression in Lyme arthritis development.

2022-02-17 | GSE181071 | GEO

Gene expression profiling during active Lyme arthritis development (22 days post infection with B. burgdorferi) in CD45 negative cells isolated from joint tissue of highly genetically similar mouse strains: B6, ISRCL4, and ISRCL3

Project description:Previously, using a forward genetic approach we identified B. burgdorferi arthritis-associated locus 1 (Bbaa1), a quantitative trait locus on Chr4, which physically encompasses the type I IFN gene cluster and regulates Lyme arthritis through heightened type I IFN production. Reciprocal radiation chimeras between B6.C3-Bbaa1 and B6 mice revealed that arthritis is initiated by radiation-sensitive cells, but orchestrated by radiation-resistant components of joint tissue. Advanced congenic lines were developed to reduce the physical size of the Bbaa1 interval, and RNA-seq of resident CD45- joint cells from advanced interval specific recombinant congenic lines (ISRCL4 and ISRCL3) identified myostatin as uniquely upregulated in association with Bbaa1 arthritis development. Our manuscript further demonstrates that myostatin expression is linked to IFN-β production, and in vivo inhibition of myostatin suppresses Lyme arthritis in the reduced interval Bbaa1 congenic mice, formally implicating myostatin as a novel downstream mediator of joint-specific inflammatory response to B. burgdorferi.

2018-02-13 | GSE102748 | GEO

Mus musculus

Project description:Expression profiling of joint tissue from C3H and interval specific congenic mouse lines post- B. burgdorferi infection

| PRJNA117207 | ENA

Gene Expression Profiling Reveals Unique Pathways Associated with Differential Severity of Lyme Arthritis

Project description:The murine model of Lyme disease provides a unique opportunity to study the localized host response to similar stimulus, B. burgdorferi, in the joints of mice destined to develop severe arthritis (C3H) or mild disease (C57BL/6). Pathways associated with the response to infection and the development of Lyme arthritis were identified by global gene expression patterns using oligonucleotide microarrays. A robust induction of IFN responsive genes was observed in severely arthritic C3H mice at one week of infection, which was absent from mildly arthritic C57BL/6 mice. In contrast, infected C57BL/6 mice displayed a novel expression profile characterized by genes involved in epidermal differentiation and wound repair, which were decreased in the joints of C3H mice. These expression patterns were associated with disease state rather than inherent differences between C3H and C57BL/6 mice, as C57BL/6-IL10-/- mice infected with B. burgdorferi develop more severe arthritis that C57BL/6 mice and displayed an early gene expression profile similar to C3H mice. Gene expression profiles at two and four weeks post infection revealed a common response of all strains that was likely to be important for the host defense to B. burgdorferi and mediated by NF-kB-dependent signaling. The gene expression profiles identified in this study add to the current understanding of the host response to B. burgdorferi and identify two novel pathways that may be involved in regulating the severity of Lyme arthritis. Keywords: disease state analysis, time course

2006-12-14 | GSE6055 | GEO

Transcription profiling of mouse model of Lyme disease

2008-06-14 | E-GEOD-6055 | biostudies-arrayexpress

Transcription profiling of mouse liver and spleen from strains that are susceptible and tolerant to trypanosome infection

Project description:Tissues were harvested from mice from two congenic strains (Tir1CC and Tir3CC) and their two control strains (Tir1AA and Tir3AA). The congenic strains were bred from inbred lines known to be susceptible (A/J) and tolerant (C57BL/6) to Trypanosome infection, such that C57BL/6 genomic regions underlying QTL for trypanotolerance were present in an A/J genetic background. Liver and spleen tissues were harvested. For each strain RNA was prepared from various tissues of twenty mice. For each condition, RNA extracts from individuals were pooled (5 per pool) prior to hybridisation.

2009-12-02 | E-TABM-865 | biostudies-arrayexpress

Bglu3 congenic mice - gene expression in liver

Project description:A congenic line was constructed by introgressing a C3H chromosome 1 region harboring Bglu3 into C57BL/6 apoE-/- background. RNA was extracted from liver using a QIAGEN kit . Total RNA was pooled in an equal amount from 3 mice for each group. Standard Affymetrix procedures were performed using 8ug of total RNA. Microarrays were used to detect gene expression in the liver of Bglu3 congenic mice and C57BL/6 apoE-deficient mouse strains fed a western diet. 2 groups of mice were studied: C57BL/6 apoE-/- control mice and Bglu3 congenic mice. After fed a Western diet for 12 weeks, liver was harvested and total RNA prepared.

2011-05-11 | E-GEOD-29151 | biostudies-arrayexpress

B31 vs rrp1 mutant

Project description:Transcriptional profiling of gene expression between parental strain B31 and rrp1 mutant. Cyclic-di-GMP is a bacterial second messenger that modulates many biological processes. Although its role in bacterial pathogenesis during mammalian infection has been widely recognized, the role of c-di-GMP in pathogen's life cycle in vector hosts is less understood. The enzootic cycle of the Lyme disease pathogen Borrelia burgdorferi involves both a mammalian host and an Ixodes tick vector. The B. burgdorferi genome encodes a single copy of the diguanylate cyclase gene (rrp1), which is responsible for the production of c-di-GMP. To determine the role of c-di-GMP in the life cycle of B. burgdorferi, an Rrp1-deficient B. burgdorferi strain was generated. The rrp1 mutant remains infectious in the mammalian host, but could not survive in the tick vector. To identify the mechanisms of Rrp1 contributing to B. burgdorferi pathogenesis and gene regulation, microarray was employed to compare gene expression profiles between the parental strain B31 and the rrp1 mutant. Two-condition experiment, B31 vs. rrp1 mutant. Biological replicates: 3 B31, 3 rrp1 mutant, independently grown and harvested. One replicate (dye-swap) per array.

2013-12-31 | E-GEOD-26968 | biostudies-arrayexpress

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