Project description:MiRNAs are involved in the pathogenesis of bronchial asthma and are involved in the regulation of airway inflammation, airway remodeling and airway hyperreactivity. In this experiment, we constructed OVA asthma model and identified the differentially expressed miRNAs in asthma and normal models by microarray technology, providing a preliminary basis for future studies on the mechanism of asthma. We used microarrays to detail the global program of gene expression in asthma models and identify miRNAs that are differentially expressed in this process.
Project description:Challenge with ovalbumin antigen is a common model for asthma in mice. We sought to identify the gene expression differences in lung tissue in naïve and OVA-sensitized mice, in response to OVA challenge.
Project description:The objective of the study was to present a transcriptome-wide m6A methylome profile of lung tissues in mouse model of ovalbumin(OVA)-induced acute allergic asthma.
Project description:Asthma bronchiale is an inflammatory disease of the respiratory airways and a major factor of increasing health care costs worldwide. The molecular actors leading to asthma are not fully understood and require further investigation. The aim of this study was to monitor the proteome during asthma development from early inflammatory to late fibrotic stages. A time-course-based ovalbumin (OVA) mouse model was applied to establish an asthma phenotype and the lung proteome was analysed at four time points during asthma development (0 weeks = control, 5 weeks, 8 weeks and 12 weeks of OVA treatment).
Project description:This program aims at identifying the lung gene signature associated with OVA-challenged mouse asthma model to facilitate understanding of the disease mechanism and therapeutic compound testing
Project description:This program aims at identifying the lung gene signature associated with OVA-challenged mouse asthma model to facilitate understanding of the disease mechanism and therapeutic compound testing The OVA-challenged profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the lungs of OVA-challenged mice compared to the corresponding PBS-treated controls.
Project description:Atopic asthma is a chronic inflammatory disease of the lungs that is commonly associated with a Th2 response. The role of allergen-specific IgG in the initiation and development of allergic airway inflammation is still poorly understood; however, a receptor of IgG-immune complexes, CD16, has been demonstrated to promote augmentation of Th2 responses. To identify what genes downstream of CD16 signaling may be contributing to development of a Th2 response, we use ovalbumin (OVA) as our model antigen and compared wildtype and CD16-/- BMDCs that were treated overnight with OVA or OVA-immune complex. C57Bl/6 and CD16-/- BMDCs were treated for 24 hours with OVA or OVA-immune complex and then analyzed for gene expression changes.
Project description:CpG-oligodeoxynucleotides (CpG-ODNs) constitute an attractive alternative for asthma treatment. We found that free feeding of an ODNcap (a CpG-ODN-embedded particle) -containing feed (ODNcap-F) prophylactically attenuates allergic airway inflammation, hyperresponsiveness, and goblet cell hyperplasia in an ovalbumin (OVA) -induced asthma model. To seek the suppressive mechanism of action of ODNcap-F in OVA-induced airway insults, we analyzed the lung transcriptome using DNA microarray analysis.
Project description:Asthma is a chronic inflammatory disease of the airways characterized by recurrent episodes of airway obstruction, hyperresponsiveness, remodeling, and eosinophilia. Phospholipase A2s (PLA2s), which release fatty acids and lysophospholipids from membrane phospholipids, have been implicated in exacerbating asthma by generating pro-asthmatic lipid mediators, but an understanding of the association between individual PLA2 subtypes and asthma is still incomplete. Here, we show that group III secreted PLA2 (sPLA2-III) plays an ameliorating, rather than aggravating, role in asthma pathology. In both mouse and human lungs, sPLA2-III was expressed in bronchial epithelial cells and decreased during the asthmatic response. In an ovalbumin (OVA)-induced asthma model, Pla2g3 knockout (-/-) mice exhibited enhanced airway hyperresponsiveness, eosinophilia, OVA-specific IgE production, and type 2 cytokine expression as compared to Pla2g3 wild-type (+/+) mice. Lipidomics analysis showed that the pulmonary levels of several lysophospholipids, including lysophosphatidylcholine, lysophosphatidylethanolamine, and lysophosphatidic acid (LPA), were decreased in OVA-challenged Pla2g3-/- mice relative to Pla2g3+/+ mice. LPA receptor 2 agonists suppressed thymic stromal lymphopoietin expression in bronchial epithelial cells and reversed airway hyperresponsiveness and eosinophilia in Pla2g3-/- mice, suggesting that sPLA2-III negatively regulates allergen-induced asthma at least by producing LPA. Thus, the activation of the sPLA2-III-LPA pathway may be a new therapeutic target for allergic asthma. Microarray gene profiling of the bronchial epithelial cells isolated from OVA-challenged lung revealed the increased expression of various chemokines and type 2 epithelial cytokines in bronchial epithelial cells from Pla2g3-/- mice as compared to those from Pla2g3+/+ mice following OVA challenge.
Project description:Atopic asthma is a chronic inflammatory disease of the lungs that is commonly associated with a Th2 response. The role of allergen-specific IgG in the initiation and development of allergic airway inflammation is still poorly understood; however, a receptor of IgG-immune complexes, CD16, has been demonstrated to promote augmentation of Th2 responses. To identify what genes downstream of CD16 signaling may be contributing to development of a Th2 response, we use ovalbumin (OVA) as our model antigen and compared wildtype and CD16-/- BMDCs that were treated overnight with OVA or OVA-immune complex.