Actinomyces sp. MAS-1
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ABSTRACT:
PROVIDER: PRJDB12084 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Macrophage activation syndrome (MAS) is a life-threatening complication of systemic juvenile idiopathic arthritis (SJIA), and increasingly reported in association with severe lung disease (SJIA-LD) of unknown etiology. This study mechanistically defines the novel observation of pulmonary inflammation in the TLR9 mouse model of MAS that recapitulate key features of SJIA-LD, including IFNg activation. In acute MAS, lungs exhibit a mild but diffuse lymphocyte-predominant perivascular, interstitial inflammation with elevated IFNg, IFN-induced chemokines, and alveolar macrophage (AMf) expression of IFNg-induced genes. However, MAS resolution demonstrated AMf expansion and increased interstitial inflammation. AMf microarrays confirmed IFNg-induced proinflammatory polarization during acute MAS, which switches towards anti-inflammatory phenotype during MAS resolution. Interestingly, recurrent MAS increased alveolar inflammation, and reset polarization towards a pro-inflammatory state. Furthermore, in mice bearing macrophages insensitive to IFNg, both systemic feature of MAS and pulmonary inflammation were markedly attenuated. These findings demonstrate experimental MAS induces IFNg-driven pulmonary inflammation, and define this system for further study of and treatment validation in SJIA-LD. We used microarrays to study whole transcriptome analysis of alveolar macrophages in the TLR9 mouse model of MAS during both acute MAS and MAS resolution.
2021-07-27 | GSE149034 | GEO
Project description:Complete genome sequence of Actinomyces sp. Chiba101
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Project description:Toxoplasma gondii MAS genome sequencing project
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Project description:Chloroplast genome of Dryopteris filix-mas
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Project description:The AT2-receptor (AT2R) and the receptor MAS are GPCRs within the renin-angiotensin-system mediating protective actions. Their unconventional signaling mechanisms are still not well characterized, but those known display a high degree of similarity. The proposed project is part of a large-scale collaboration with the group of Robson Santos, a leader in Ang1-7/MAS research, aiming at a better characterization of AT2R-MAS signaling and crosstalk. Building up on our finding that the AT2R and MAS heterodimerise and on the mapping of the entire Ang-(1−7)/MAS signaling network by the Santos group, the proposed studies will look at AT2R-MAS signaling in two ways: mapping the AT2R signaling network by quantitative phosphoproteomics and compare it with the MAS network.
2022-11-18 | PXD005802 | Pride
Project description:Oral streptococci, including Streptococcus gordonii, and Actinomyces naeslundii, are consistently found to be the most abundant bacteria in the early stages of dental plaque accumulation. These organisms interact physically (coaggregate) in vitro and in vivo. We hypothesized that coaggregation between S. gordonii and A. naeslundii leads to changes in gene expression in the partner organisms. Furthermore, we predicted that coaggregation-induced changes in phenotype contribute to the success of streptococci and actinomyces in dental plaque. To assess the responses of S. gordonii to coaggregation with A. naeslundii, RNA was extracted from S. gordonii cells 3 h after inducing coaggregation with A. naeslundii or from equivalent S. gordonii monocultures. The two RNA populations were reverse transcribed and compared by competitive hybridization with an S. gordonii genomic microarray. The most striking feature of the response to coaggregation was a profound change in expression of S. gordonii genes involved in arginine biosynthesis and transport. Subsequent experiments demonstrated that coaggregation with A. naeslundii stabilizes arginine biosynthesis in S. gordonii and enables growth under low-arginine conditions, such as those present in human saliva. Keywords: Cell-cell interaction
2008-06-02 | GSE9478 | GEO