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Levofloxacin induces the downexpression of inflammation-related transcriptome in the gut of spondyloarthritis DBA/1 mice.

ABSTRACT: Levofloxacin induces the downexpression of inflammation-related transcriptome in the gut of spondyloarthritis DBA/1 mice.

PROVIDER: PRJNA892511 | ENA |

REPOSITORIES: ENA

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Levofloxacin induces the downexpression of inflammation-related transcriptome in the gut of spondyloarthritis DBA/1 mice.

Project description:Gene expression profiles in the gut of DBA/1 mice whit spontaneus arthritis and treated with levofloxacion vs. those who were not received levofloxacin were compared. Levofloxacin induced the downexpression of inflammation-related genes and signaling pathways.

2022-10-22 | GSE216174 | GEO

Levofloxacin induces the downexpression of inflammation-related transcriptome in the spine of spondyloarthritis DBA/1 mice.

Project description:Gene expression profiles in the spine of DBA/1 mice whit spontaneus arthritis and treated with levofloxacion vs. those who were not received levofloxacin were compared. Levofloxacin induced the downexpression of inflammation-related genes and signaling pathways.

2022-10-22 | GSE216173 | GEO

Levofloxacin induces the downexpression of inflammation-related transcriptome in the tarsal joint of Spondyloarthritis DBA/1 mice.

Project description:Gene expression profiles in the tarsal joints of DBA/1 mice whit spontaneus arthritis and treated with levofloxacion vs. those who were not received levofloxacin were compared. Levofloxacin induced the downexpression of inflammation-related genes and signaling pathways.

2022-10-22 | GSE216172 | GEO

Levofloxacin induces the downexpression of inflammation-related transcriptome in the spine of spondyloarthritis DBA/1 mice.

Project description:Levofloxacin induces the downexpression of inflammation-related transcriptome in the spine of spondyloarthritis DBA/1 mice.

| PRJNA892512 | ENA

Levofloxacin induces the downexpression of inflammation-related transcriptome in the tarsal joint of Spondyloarthritis DBA/1 mice.

Project description:Levofloxacin induces the downexpression of inflammation-related transcriptome in the tarsal joint of Spondyloarthritis DBA/1 mice.

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Gene expression profile of the age-related hearing loss cochlea in DBA/2J mice

Project description:Age-related hearing loss (AHL) is the progressive loss of auditory function with aging. The DBA/2J (DBA) mice have been used as a model of AHL and undergoes progressive, age-related hearing loss by 12 weeks of age. Here we analyzed cochlear gene expression of 7-week-old and 36-week-old DBA mice using microarrays. Auditory brainstem response (ABR) analysis confrimed that severe age-related hearing loss occured in 36-week-old mice, whereas moderate hearing loss occured in 7-week-old mice. Comprehensive gene expression analysis identified genes correlated with AHL and revealeed that 15 mitochondrial process categories, including “mitochondrial electron transport chain”, “oxidative phosphorylation”, “respiratory chain complex I”, “respiratory chain complex IV”, and “respiratory chain complex V”, were statistically associated with AHL-correlated genes in the cochlea of 36-week-old DBA mice, and that 25 genes encoding components of the mitochondrial respiratory chain (respiratory chain complex I, IV, and V) were significantly down-regulated in the cochlea. These observations provide evidence that AHL is associated with down-regulation of genes involved in the mitochondrial respiratory chain in the cochlea of DBA mice, and suggest that mitochondrial respiratory chain dysfunction may be a key feature of AHL in mammalian cochlea. Keywords: Disease state analysis, Time course analysis

2007-10-16 | GSE6045 | GEO

Proteomics analysis of plasma from radiographic axial spondyloarthritis patients.

Project description:Tandem mass spectrometry analysis of proteins from depleted plasma from radiographic axial spondyloarthritis patients pre- and post-treated with adalimumab.

2024-05-02 | PXD026189 | Pride

Gene expression in juvenile spondyloarthritis

Project description:Association of juvenile spondyloarthritis (jSpA) with the HLA-B27 genotype is well established, but there is little knowledge of other genetic factors with a role in disease development. The aim of the present study was to identify and confirm gene signatures and novel biomarkers in various cohorts of untreated and treated patients diagnosed with jSpA and other forms of juvenile idiopathic arthritis (JIA). DNA microarray gene expression was performed in 11 patients with jSpA and in four healthy controls, along with bioinformatics analysis of retrieved data (DAVID, GSEA, IPA).

2014-10-31 | GSE58667 | GEO

Metagenomic Spondyloarthritis

Project description:Reciprocal inlfuence of TNF alpha inhibitor and microbiota composition in spondyloarthritis patients

| PRJEB19186 | ENA

Distinct immune modulatory roles of regulatory T cells in gut versus joint inflammation in TNF driven spondyloarthritis [II]

Project description:Objectives: Gut and joint inflammation commonly co-occur in spondyloarthritis (SpA) which strongly restricts therapeutic modalities. The immunobiology underlying differences between gut and joint immune regulation, however, is poorly understood. We therefore assessed the immunoregulatory role of CD4+FOXP3+ regulatory T (Treg) cells in a model of Crohn’s-like ileitis and concomitant arthritis. Methods: RNA-sequencing (RNA-seq) and flow cytometry were performed on inflamed gut and joint samples and tissue-derived Tregs from TNF∆ARE mice. In situ hybridization of TNF and its receptors (TNFR) was applied to human SpA gut biopsies. Soluble(s) TNFR levels were measured in serum of mice and SpA patients and controls. Treg function was explored by in vitro co-cultures and in vivo by conditional Treg depletion. Results: Chronic TNF exposure induced several TNF superfamily (TNFSF) members (4-1BBL, TWEAK and TRAIL) in synovium and ileum in a site-specific manner. Elevated TNFR2 mRNA levels were noted in TNF∆ARE/+ mice leading to increased sTNFR2 release. Likewise, sTNFR2 levels were higher in SpA patients with gut inflammation and distinct from inflammatory and healthy controls. Tregs accumulated at both gut and joints of TNF∆ARE mice, yet their TNFR2 expression and suppressive function was significantly lower in synovium versus ileum. In line herewith, synovial and intestinal Tregs displayed a distinct transcriptional profile with tissue restricted TNFSF receptor and p38MAPK gene expression. Conclusions: These data point to profound differences in immune-regulation between Crohn’s ileitis and peripheral arthritis. Whereas Tregs control ileitis they fail to dampen joint inflammation. Synovial resident Tregs are particularly maladapted to chronic TNF exposure.

2023-05-22 | GSE232406 | GEO

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