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Inos_pseudomonas

ABSTRACT: Human Airway Epithelium Controls Pseudomonas aeruginosa Infection via inducible Nitric Oxide Synthase

PROVIDER: PRJEB82833 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13998991.fastq.gz	Fastqsanger.gz
	ERR13998992.fastq.gz	Fastqsanger.gz
	ERR13998993.fastq.gz	Fastqsanger.gz
	ERR13998994.fastq.gz	Fastqsanger.gz
	ERR13998995.fastq.gz	Fastqsanger.gz

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Overexpression of Dimethylarginine Dimethylaminohydrolase 1 Attenuates Airway Inflammation in Mouse Models of Asthma

Project description:Levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, are increased in lung, sputum, exhaled breath condensate and plasma samples from asthma patients. ADMA is metabolized primarily by dimethylarginine dimethylaminohydrolase 1 (DDAH1) and DDAH2. We determined the effect of DDAH1 overexpression on development of allergic inflammation in mouse models of asthma. Wild type and DDAH1-transgenic mice were challenged with PBS or house dust mite (HDM). Airway inflammation was assessed by bronchoalveolar lavage (BAL) total and differential cell counts. Gene expression in lungs was determined by RNA-Seq and RT-quantitative PCR (qPCR). The expression of DDAH1 and DDAH2 was decreased in the lungs of mice following HDM exposure. Transgenic overexpression of DDAH1 resulted in decreased BAL total cell and eosinophil numbers following HDM exposure. Total IgE levels in serum and BAL fluid were decreased in HDM-exposed DDAH1-transgenic mice compared to HDM-exposed wild type mice. RNA-Seq results showed downregulation of genes in inducible nitric oxide synthase (iNOS) signaling pathway in PBS-treated DDAH1 transgenic mice versus PBS-treated wild type mice and downregulation of genes in IL-13/FOXA2 signaling pathway in HDM-treated DDAH1 transgenic mice versus HDM-treated wild type mice. Our findings suggest that decreased expression of DDAH1 in airway epithelial cells may contribute to allergic asthma and overexpression of DDAH1 attenuates allergen-induced airway inflammation through modulation of Th2 responses. mRNA profiles of WT and DDAH1-transgenic mice treated with PBS or house dust mite (HDM).

2013-12-03 | E-GEOD-49047 | biostudies-arrayexpress

Dataset 2: Targets of SCoR-mediated Denitrosylation

Project description:Identification of targets of SNO-CoA- and SCoR-mediated denitrosylation in HEK293 cells expressing inducible nitric oxide synthase.

2018-12-11 | PXD011881 | Pride

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Project description:To describe the transcriptional changes associated with polymicrobial-sepsis induced myocardial depression in wild type and iNOS deficient mice. Keywords: myocardium, contractility, differential gene expression, nitric oxide synthase, infection

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Project description:DNA microarray analysis was employed to investigate the transcriptome response to nitric oxide in Pseudomonas aeruginosa. We focused on the role played by the nitric oxide-response regulators DNR and FhpR and an oxygen-response regulator ANR in the response. The transcriptome profiles of the P. aeruginosa strains before and after exposure to nitric oxide under the microaerobic conditions were analyzed. Wild type, its anr, dnr, and fhpR mutants, and the anr mutant that express dnr were used for the analyses. Pseudomonas aeruginosa wild type (PAO1ut), anr mutant (RManr), dnr mutant (RMdnr), anr mutant that constitutively expresses DNR (RManrEXdnr), and fhpR mutant (PDM2665) were cultivated microaerobically in LB in 1-liter jar fermenter. When optical density at 600 nm reached 0.3, nitric oxide-saturated water was added to the medium (final nitric oxide concentration was 20 micro-M). RNA was isolated from a 10 ml aliquot of the culture prior to the addition of nitric oxide and at 5 min after the addition. The experiment was performed in duplicate independent cultures.

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Project description:Inducible nitric oxide synthase (iNOS) plays a crucial role in controlling growth of mycobacteria, presumed to be via nitric oxide (NO) mediated killing. However, NOS enzymes can also signal through NO-independent pathways, and production of NO by NOS requires the cofactor tetrahydrobiopterin (BH4). We compared Nos2-/- mice to mice with macrophage BH4 deficiency (Gch1fl/flTie2cre), due to a leukocyte-specific deletion of Gch1, to uncover the specific contribution of NO-independent NOS functions to anti-mycobacterial immunity. We used microarrays to detail the global programme of gene expression in uninfected and BCG infected macrophages that were either deficient in iNOS (Nos2-/- vs C57bl6/J) or BH4/Gch1 (GCHfl/flTie2cre vs GCHfl/fl)

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Project description:Classical stimulation of macrophages (MLPS/IFNγ) elicits the expression of inducible nitric oxide synthase (iNOS), generating large amounts of nitric oxide (NO) and inhibiting respiration. Consequent upregulation of glycolysis and a disrupted tricarboxylic acid (TCA) cycle underpin this switch to a pro-inflammatory phenotype. Here we show that the NOS cofactor tetrahydrobiopterin (BH4) modulates key aspects of metabolic remodelling in activated bone-marrow-derived macrophages (BMDMs) via NO production. Using two complementary mouse models that each lack the capacity for inducible NO generation, through different mechanisms, we reveal that NO regulates macrophage respiratory function via changes in the abundance of critical N-module subunits in Complex I, by HIF1α-mediated glycolytic remodelling, and by modulating levels of the critical TCA cycle metabolites, and inflammatory mediators, citrate, succinate, and itaconate. Taken together, our findings reveal new critical roles for iNOS-derived NO that are required for metabolic remodelling and cytokine production in macrophage inflammatory responses.

2019-05-31 | PXD010628 | Pride

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