Expression analysis of inflammatory cytokines in exhaled breath condensates from pediatric patients with sickle cell disease, asthma, sickle cell disease and asthma, and controls
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PROVIDER: PRJNA631006 | ENA |
REPOSITORIES: ENA
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Project description:To analyze expression of inflammatory cytokines in Exhaled Breath Condensates from pediatric patients with sickle cell disease, asthma, sickle cell disease and asthma, and controls
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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
Project description:Sickle cell disease is a growing health burden afflicting millions around the world. Clinical observation and laboratory studies have shown that the severity of sickle cell disease is ameliorated in individuals who have elevated levels of fetal hemoglobin. However, pharmacologic induction of fetal hemoglobin sufficient to diminish clinical severity in sickle patients has been challenging. We recently found that up-regulation of PGC-1α can induce fetal hemoglobin synthesis in human primary erythroblasts. Here, we report that a small molecular compound SR-18292 increases PGC-1α leading to enhanced fetal hemoglobin expression in human erythroid cells or β-YAC and sickle cell disease mice. Sickled red blood cells are significantly reduced and disease complications are alleviated in SR-18292-treated sickle mice. SR-18292, or agents in its class, could be a promising therapeutic for sickle cell disease.
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Project description:Polymorphonuclear neutrophils are key actors in the pathophysiology of sickle cell disease, but specific factors underlying their activation and sustained inflammation are not well documented. In the present study, we investigated the proteome of neutrophils by a label-free global comparative approach between 4 non-treated sickle patients (SS genotype) at steady state and 4 healthy donors. We identified 101 proteins differentially expressed in SS and normal neutrophils. We found overexpression of CD64 and under-expression of CD62L suggestive of an activated and aged neutrophil profile in SS patients. Comparison of the two proteomes revealed a strong involvement of the type 1 interferon (IFN) response pathway with a 3- to 84-fold increase of type 1 IFN-induced proteins in SS neutrophils, and overexpression of STAT1 and STAT2. Thus, we next determined the plasmatic concentration of type 1 IFNs (IFNα and IFNβ) using the digital-ELISA technology and found a significant higher concentration of IFNα in the plasma from half of our SS patients compared to controls. Overall, a dramatic high-level expression of IFNα signaling proteins in neutrophils from SS patients suggests auto-inflammatory-like phenotype in sickle cell disease at steady state. This finding could open the way to new anti-inflammatory therapies.
2020-11-11 | PXD014457 | Pride
Project description:BACKGROUND: Evaluation of the airway transcriptome may reveal patterns of gene expression that are associated with clinical phenotypes of asthma. To define transcriptomic endotypes of asthma (TEA) we analyzed gene expression in induced sputum that correlate with phenotypes of disease. METHODS: Gene expression was measured in sputum of subjects with asthma using Affymetrix HuGene ST 1.0 microarrays. Unsupervised clustering analysis of genes in pathways selected from the Kyoto Encyclopedia of Genes and Genomes (KEGG) identified TEA clusters. Clinical characteristics were compared and logistic regression analysis of matched blood samples defined an expression profile to determine the TEA cluster assignment in a cohort of children with asthma for validation. RESULTS: Three TEA clusters were identified. TEA cluster 1 had the most subjects with a history of intubation (P = 0.05), a lower pre-bronchodilator FEV1 (P = 0.006), a higher bronchodilator response (P = 0.03), and higher exhaled nitric oxide levels (P = 0.04), compared to the other TEA clusters. TEA cluster 2, the smallest cluster had the most subjects that were hospitalized for asthma (P = 0.04). Subjects in TEA cluster 3, the largest cluster, had normal lung function, low exhaled nitric oxide levels, and lower inhaled steroid requirements. Evaluation of TEA clusters in children confirmed that TEA clusters 1 and 2 are associated with a history of intubation (P = 5.58 x 10-06) and hospitalization (P = 0.01), respectively. CONCLUSIONS: Patterns of gene expression in the sputum and blood reveal TEA clusters that are associated with severe asthma phenotypes in children and adults. Gene expression was measured in sputum of subjects with asthma using Affymetrix HuGene ST 1.0 microarrays. Unsupervised clustering analysis of genes in pathways selected from the Kyoto Encyclopedia of Genes and Genomes (KEGG) identified TEA clusters. Clinical characteristics were compared and logistic regression analysis of matched blood samples defined an expression profile to determine the TEA cluster assignment in a cohort of children with asthma for validation.
2014-04-07 | E-GEOD-56396 | biostudies-arrayexpress
Project description:The establishment and public sharing of comprehensive proteome maps of human tissues and biofluids are essential to improve biomedical knowledge and to support biomarker discovery studies. In this study, we performed an in-depth proteomics characterization of the exhaled breath condensate (EBC), a non-invasive sample obtained from the condensation of the airway lining fluid. Two pooled samples of EBC, each combined from 10 healthy donors, were lyophilized and their protein content analyzed by high-resolution tandem mass spectrometry-based proteomics. Two “technical” negative control samples were processed in parallel with the pooled samples to correct for exogenous protein contamination and avoid erroneous identifications.
2017-12-06 | PXD007591 | Pride